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A comprehensive review on magnetic carbon nanotubes and carbon nanotube-based buckypaper for removal of heavy metals and dyes

Khan FSA, Mubarak NM, Tan YH, Khalid M, Karri RR, Walvekar R, et al.

J Hazard Mater, 2021 07 05;413:125375.
PMID: 33930951 DOI: 10.1016/j.jhazmat.2021.125375

Industrial effluents contain several organic and inorganic contaminants. Among others, dyes and heavy metals introduce a serious threat to drinking waterbodies. These pollutants can be noxious or carcinogenic in nature, and harmful to humans and different aquatic species. Therefore, it is of high importance to remove heavy metals and dyes to reduce their environmental toxicity. This has led to an extensive research for the development of novel materials and techniques for the removal of heavy metals and dyes. One route to the removal of these pollutants is the utilization of magnetic carbon nanotubes (CNT) as adsorbents. Magnetic carbon nanotubes hold remarkable properties such as surface-volume ratio, higher surface area, convenient separation methods, etc. The suitable characteristics of magnetic carbon nanotubes have led them to an extensive search for their utilization in water purification. Along with magnetic carbon nanotubes, the buckypaper (BP) membranes are also favorable due to their unique strength, high porosity, and adsorption capability. However, BP membranes are mostly used for salt removal from the aqueous phase and limited literature shows their applications for removal of heavy metals and dyes. This study focuses on the existence of heavy metal ions and dyes in the aquatic environment, and methods for their removal. Various fabrication approaches for the development of magnetic-CNTs and CNT-based BP membranes are also discussed. With the remarkable separation performance and ultra-high-water flux, magnetic-CNTs, and CNT-based BP membranes have a great potential to be the leading technologies for water treatment in future.

Matched MeSH terms: Carcinogens
Manual work and lung cancer risk in high-risk populations

Fauziah Nordin, Lewis, SJ., O’Donnell, PNS., Crosbie, PAJ., Richard Booton, Agius, RM., et al.

Journal of Occupational Safety and Health, 2014;11(1):5-14.
MyJurnal

Manual work is associated with increased lung cancer risk possibly because of increased exposure to occupational and other carcinogens, reduced use of health care services and/or a less healthy lifestyle. The aim of this study was to examine whether the association between manual work and lung cancer risk has changed over time. Three separate retrospective studies were carried out over a 10-year period (1996-1997, 1998-2000 and 2003-2005) in patients attending a bronchoscopy clinic to investigate lung cancer risk in an area of Manchester characterised by high deprivation and unemployment. Cases (n=321) were patients newly diagnosed with a tumour of the lung, trachea or bronchus and controls (n=542) were patients free of tumours at the time of, and prior to, examination. Patients were interviewed using the same structured questionnaire for associations between risk factors and lung cancer examined. The study population in all three studies was similar with little difference in smoking history. In each study smoking was associated with lung cancer risk. Lung cancer risk was higher in manual workers (compared to managers and other professionals) in the first (OR 2.50, 95% CI 1.20 – 5.05) and second study (OR 2.73, 95% CI 0.97 – 7.70) but not the third (OR 0.97, 95% CI 0.58 – 1.61). However, the summary odds ratio (meta-OR) for lung cancer in manual worker was 1.81 (95% 1.75 – 1.87) after controlling for sex, age and smoking. This study suggested that even after taking into account known occupational and environmental causes of cancer, there was a residual cancer risk associated with manual work, high risk working populations of lung cancer. However this appears to have attenuated recently for as yet unknown reasons.

Matched MeSH terms: Carcinogens
Fulltext FGFR3 mutation increases bladder tumourigenesis by suppressing acute inflammation

Foth M, Ismail NFB, Kung JSC, Tomlinson D, Knowles MA, Eriksson P, et al.

J Pathol, 2018 Nov;246(3):331-343.
PMID: 30043421 DOI: 10.1002/path.5143

Recent studies of muscle-invasive bladder cancer show that FGFR3 mutations are generally found in a luminal papillary tumour subtype that is characterised by better survival than other molecular subtypes. To better understand the role of FGFR3 in invasive bladder cancer, we examined the process of tumour development induced by the tobacco carcinogen OH-BBN in genetically engineered models that express mutationally activated FGFR3 S249C or FGFR3 K644E in the urothelium. Both occurrence and progression of OH-BBN-driven tumours were increased in the presence of an S249C mutation compared to wild-type control mice. Interestingly, at an early tumour initiation stage, the acute inflammatory response in OH-BBN-treated bladders was suppressed in the presence of an S249C mutation. However, at later stages of tumour progression, increased inflammation was observed in S249C tumours, long after the carcinogen administration had ceased. Early-phase neutrophil depletion using an anti-Ly6G monoclonal antibody resulted in an increased neutrophil-to-lymphocyte ratio at later stages of pathogenesis, indicative of enhanced tumour pathogenesis, which supports the hypothesis that suppression of acute inflammation could play a causative role. Statistical analyses of correlation showed that while initial bladder phenotypes in morphology and inflammation were FGFR3-dependent, increased levels of inflammation were associated with tumour progression at the later stage. This study provides a novel insight into the tumour-promoting effect of FGFR3 mutations via regulation of inflammation at the pre-tumour stage in the bladder. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Matched MeSH terms: Carcinogens
Fulltext Proximate analysis, mineral content and antioxidant capacity of milk apple, malay apple and water apple

Lim, A.S.L., Rabeta, M.S.

International Food Research Journal, 2013;20(2):673-679.
MyJurnal

The aim of this study is to determine the antioxidant capacity of underutilized fruits in Malaysia namely Milk apple (Syzygium malaccense), Malay apple (Syzygium malaccense (L.) Merr. and Perry), and Water apple (Syzygium aqueum). Synthetic antioxidants (BHA and BHT) commonly used in the food industries may not be as safe as it was presumed earlier. As BHA and BHT may be carcinogenic, it is important to look for new sources of natural antioxidants from fruits and vegetables. Freeze dried samples extracted with acetone and water were measured by ferric 1, 1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging and Ferric Reducing Antioxidant Power (FRAP) assays. Acetone extract (50%) showed higher values for both DPPH and FRAP assays compared with water extract. Milk apple has the highest DPPH value of 95.26% inhibition of DPPH. Milk apple also showed the highest FRAP value with 8722.22 µM of Fe (II) per gram of freeze dried sample. There was a significant difference (P < 0.05) in the types of extraction used. Antioxidant capacities of the samples are in the following order: Milk apple > Malay apple > Water apple. Proximate compositions and mineral contents of the samples were determined too. The samples can be used as a source of natural antioxidants.

Matched MeSH terms: Carcinogens
The improvement of in vivo model (Balb/c mice) for cervical carcinogenesis using diethylstilbestrol (DES)

Zulfahmi S, Yazan LS, Ithnin H, Armania N

Exp. Toxicol. Pathol., 2013 Nov;65(7-8):1083-9.
PMID: 23726752 DOI: 10.1016/j.etp.2013.04.004

Cervical cancer is the most common gynecological cancer and one of the major causes of female cancer-related death worldwide particularly in developing countries. Thus far, there are a few in vivo models have been developed in investigating this type of cancer. In this study, we induced cervical cancer in Balb/c mice by exploiting the carcinogenic property of diestylstilbestrol (DES). The Balb/c pregnant mice were given subcutaneous (SC) injection of 67μg/kg body weight of DES on GD 13, and the mice gave birth approximately at gestation day 19-22. Female offspring were reared and the body weight was recorded once weekly. The female offspring were sacrificed at age of 5 months. Upon termination, blood was collected in a plain tube via cardiac puncture and the reproductive tracts were collected and weighed. The reproductive tract sections were stained using H&E for observation of pathological changes. The progression of disease state was monitored by measuring the level of serum interleukin (IL-6) using the Mouse IL-6 ELISA Assay Kit (BD OptEIA™, USA). All parameters were compared with Not-induced group. The outcome of this study demonstrated a significant difference in body weight gain, reproductive organ weight, diameter of cervix and the level of serum IL-6 in the Induced group as compared to the Not-induced group (P<0.05). Histopathological findings revealed the presence of adenosis only in the Induced group. It shows that DES could be employed as an agent to induce cervical carcinogenesis in animal model. In addition to that, new potential anti-cancer agents from various sources could be further evaluated using this technique.

Matched MeSH terms: Carcinogens/toxicity*
Kenaf seed supercritical fluid extract reduces aberrant crypt foci formation in azoxymethane-induced rats

Ghafar SA, Yazan LS, Tahir PM, Ismail M

Exp. Toxicol. Pathol., 2012 Mar;64(3):247-51.
PMID: 20869858 DOI: 10.1016/j.etp.2010.08.016

Kenaf (Hibiscus cannabinus) a plant of the family Malvaceae, is a valuable fiber plant native to India and Africa. Kenaf seeds contain alpha-linolenic acid, phytosterol such as β-sitosterol, vitamin E and other antioxidants with chemopreventive properties. In the present study we examined the hypothesis that kenaf seed 'supercritical fluid extract' (SFE) extract could suppress the early colon carcinogenesis in vivo by virtue of its bioactive compounds. To accomplish this goal, 60 male rats were randomly assigned to 5 groups which were (1) negative control group [not induced with azoxymethane (AOM)]; (2) positive control group (induced with AOM but received no treatment); (3) group treated with 500 mg/kg kenaf seed SFE extract; (4) group treated with 1000 mg/kg kenaf seed SFE extract; (5) group treated with 1500 mg/kg kenaf seed SFE extract. At 7 weeks of age, all rats except the negative control group received 15 mg/kg of AOM injection subcutaneously once a week for 2 weeks. Rats were euthanized at 13 weeks of the experiment. Number of ACF (mean±SD) ranged from 84.4±4.43 to 179.5±12.78 in group 2, 3, 4, 5. ACF reductions compared with the untreated group were 45.3, 51.4 and 53.1% in rats fed with 500, 1000 and 1500 mg/kg body weight, respectively. There were no significant differences in weight gain among groups. Our finding indicates that kenaf seed SFE extract reduced AOM-induced ACF in Sprague-Dawley male rats.

Matched MeSH terms: Carcinogens/toxicity
Anticarcinogenic efficacy of phytic acid extracted from rice bran on azoxymethane-induced colon carcinogenesis in rats

Norazalina S, Norhaizan ME, Hairuszah I, Norashareena MS

Exp. Toxicol. Pathol., 2010 May;62(3):259-68.
PMID: 19464858 DOI: 10.1016/j.etp.2009.04.002

This study is carried out to determine the potential of phytic acid extracted from rice bran in the suppression of colon carcinogenesis induced by azoxymethane (AOM) in rats. Seventy-two male Sprague-Dawley rats were divided into 6 groups with 12 rats in each group. The intended rats for cancer treatment received two intraperitoneal injections of AOM in saline (15mg/kg bodyweight) over a 2-week period. The treatments of phytic acid were given in two concentrations: 0.2% (w/v) and 0.5% (w/v) during the post-initiation phase of carcinogenesis phase via drinking water. The colons of the animals were analyzed for detection and quantification of aberrant crypt foci (ACF) after 8 weeks of treatment. The finding showed treatment with 0.2% (w/v) extract phytic acid (EPA) gave the greatest reduction in the formation of ACF. In addition, phytic acid significantly suppressed the number of ACF in the distal, middle and proximal colon as compared to AOM alone (p<0.05). For the histological classification of ACF, treatment with 0.5% (w/v) commercial phytic acid (CPA) had the highest percentage (71%) of non-dysplastic ACF followed by treatment with 0.2% (w/v) EPA (61%). Administration of phytic acid also reduced the incidence and multiplicity of total tumors even though there were no significant differences between groups. In conclusion, this study found the potential value of phytic acid extracted from rice bran in reducing colon cancer risk in rats.

Matched MeSH terms: Carcinogens/toxicity
Fulltext Environmental immune disruptors, inflammation and cancer risk

Thompson PA, Khatami M, Baglole CJ, Sun J, Harris SA, Moon EY, et al.

Carcinogenesis, 2015 Jun;36 Suppl 1:S232-53.
PMID: 26106141 DOI: 10.1093/carcin/bgv038

An emerging area in environmental toxicology is the role that chemicals and chemical mixtures have on the cells of the human immune system. This is an important area of research that has been most widely pursued in relation to autoimmune diseases and allergy/asthma as opposed to cancer causation. This is despite the well-recognized role that innate and adaptive immunity play as essential factors in tumorigenesis. Here, we review the role that the innate immune cells of inflammatory responses play in tumorigenesis. Focus is placed on the molecules and pathways that have been mechanistically linked with tumor-associated inflammation. Within the context of chemically induced disturbances in immune function as co-factors in carcinogenesis, the evidence linking environmental toxicant exposures with perturbation in the balance between pro- and anti-inflammatory responses is reviewed. Reported effects of bisphenol A, atrazine, phthalates and other common toxicants on molecular and cellular targets involved in tumor-associated inflammation (e.g. cyclooxygenase/prostaglandin E2, nuclear factor kappa B, nitric oxide synthesis, cytokines and chemokines) are presented as example chemically mediated target molecule perturbations relevant to cancer. Commentary on areas of additional research including the need for innovation and integration of systems biology approaches to the study of environmental exposures and cancer causation are presented.

Matched MeSH terms: Carcinogens, Environmental/adverse effects*
Vitamin E, glutathione S-transferase and gamma-glutamyl transpeptidase activities in cultured hepatocytes of rats treated with carcinogens

Ong FB, Wan Ngah WZ, Top AG, Khalid BA, Shamaan NA

Int. J. Biochem., 1994 Mar;26(3):397-402.
PMID: 7910569

1. The effects of alpha-tocopherol and gamma-tocotrienol on glutathione S-transferase (GST) and gamma-glutamyl transpeptidase (gamma-GT) activities in cultured hepatocytes prepared from rats treated with diethylnitrosamine (DEN) and 2-acetylaminofluorene (AAF) were investigated. 2. Both the alpha-tocopherol and gamma-tocotrienol treated hepatocytes showed significantly higher (P < 0.05) GST activities than untreated hepatocytes prepared from the carcinogen treated rats in the first 3 days of culture. Treatment with alpha-tocopherol and gamma-tocotrienol generally resulted in a tendency to increase the GST activities above that in the untreated hepatocytes. 3. Treatment with high doses (125-250 microM) of alpha-tocopherol and low doses (12.5-25 microM) of gamma-tocotrienol generally resulted in a significant reduction in gamma-GT activities at 1-3 days. gamma-GT activities are reduced as the dose of alpha-tocopherol and gamma-tocotrienol are increased.

Matched MeSH terms: Carcinogens/toxicity*
Effect of ovariectomy and sex hormones replacement on tumour marker enzymes under administration of chemical carcinogens in the rat

Zarida H, Wan Zurinah WN, Zanariah J, Michael LK, Khalid BA

Exp. Toxicol. Pathol., 1994 Mar;46(1):31-6.
PMID: 7916223

The effect of ovariectomy and sex hormone/s replacement in female rats was investigated by the determination of the tumour marker enzymes gamma-glutamyltranspeptidase (GGT) and alkaline phosphatase (ALP). This was compared to ovariectomized rats receiving sex hormone replacement and treated with carcinogen. Ovariectomy significantly increased the activity of plasma GGT. Plasma and microsomal ALP and microsomal GGT were unchanged. When replacements of estrogen (E), or progesterone (Prog), or combinations of both estrogen and progesterone were given to ovariectomized rats, the activity of plasma GGT was brought to the level of normal intact females. Treatment with carcinogen increased the PGGT activities in intact rats. In ovariectomized rats receiving carcinogen, the PGGT activities were significantly lower than in intact females and rats receiving both hormone replacement and carcinogen (p < 0.01). Carcinogen treatment in case of estrogen or progesterone replacement, either individually or in combination, showed GGT activities comparable to intact females receiving carcinogen. Both plasma and microsomal ALP were not affected by carcinogen administration. These results showed that ovariectomy reduced the severity of hepatocarcinogenesis while sex hormone replacement worsened the process.

Matched MeSH terms: Carcinogens/pharmacology*
Antagonistic effects of styrylpyrone derivative (SPD) on 7,12-dimethylbenzanthracene-induced rat mammary tumors

Hawariah A, Stanslas J

In Vivo, 1998 Jul-Aug;12(4):403-10.
PMID: 9706492

Early studies reported that a styrylpyrone derivative (SPD) purified from the Goniothalamus sp. acts as a non-competitive antiestrogen in early pregnant mice (1). In the immature rat uterine wet weight test, we found that SPD markedly reduced uterine weight at doses 1 and 100 mg/kg, thus reflecting negative antiestrogenicity, probably attributed to low binding affinities towards ER. Tamoxifen (Tam) on the other hand exhibited partial antiestrogenicity at all doses (0.01-10 mg/kg BW) and dose-dependent estrogenicity. However, the estrogen antagonism: agonism ratio for SPD is much higher than Tam, which is indicative of the breast cancer antitumor activity as seen in compounds such as MER-25. Pretreatment assessment on 1 mg/kg BW SPD and Tam showed that SPD is not a very good, estrogen antagonist compared to Tam, as it was unable to revert the estrogenicity effect of estradiol benzoate (EB) on immature rat uterine weight. Antitumor activity assessment for SPD exhibited significant tumor growth retardation in 7,12-dimethyl benzanthracene (DMBA) induced rat mammary tumors at all doses employed (2, 10 and 50 mg/kg) compared to the controls (p < 0.01). This compound was found to be more potent than Tam (2 and 10 mg/kg) and displayed greater potency at a dose of 10 mg/kg. It caused complete remission of 33.3% of tumors but failed to prevent onset of new tumors. However, SPD administration at 2 mg/kg caused 16.7% complete remission and partial remission. It also prevented the onset of new tumors throughout the experiment.

Matched MeSH terms: Carcinogens/pharmacology
Fulltext Modulation of cancer signalling pathway(s) in two -stage mouse skin tumorigenesis by annonacin

Md Roduan MR, Abd Hamid R, Mohtarrudin N

BMC Complement Altern Med, 2019 Sep 03;19(1):238.
PMID: 31481122 DOI: 10.1186/s12906-019-2650-1

BACKGROUND: Annonacin, an annonaceous acetogenin isolated from Annona muricata has been reported to be strongly cytotoxic against various cell lines, in vitro. Nevertheless, its effect against in vivo tumor promoting activity has not been reported yet. Therefore, this study was aimed to investigate antitumor-promoting activity of annonacin via in vivo two-stage mouse skin tumorigenesis model and its molecular pathways involved.
METHODS: Mice were initiated with single dose of 7,12-dimethylbenz[α]anthracene (DMBA) (390 nmol/100 μL) followed by, in subsequent week, repeated promotion (twice weekly; 22 weeks) with 12-O-tetradecanoylphorbol-13-acetate (TPA) (1.7 nmol/100 μL). Annonacin (85 nM) and curcumin (10 mg/kg; reference) were, respectively, applied topically to DMBA/TPA-induced mice 30 min before each TPA application for 22 weeks. Upon termination, histopathological examination of skin, liver and kidney as well as genes and proteins expression analysis were conducted to elucidate the potential mechanism of annonacin.
RESULTS: With comparison to the carcinogen control, Annonacin significantly increased the tumor latency period and reduced the tumor incidence, tumor burden and tumor volume, respectively. In addition, it also suppressed tumorigenesis manifested by significant reduction of hyperkeratosis, dermal papillae and number of keratin pearls on skin tissues. Annonacin also appeared to be non-toxic to liver and kidney. Significant modulation of both AKT, ERK, mTOR, p38, PTEN and Src genes and proteins were also observed in annonacin-targeted signaling pathway(s) against tumorigenesis.
CONCLUSIONS: Collectively, results of this study indicate that annonacin is a potential therapeutic compound targeting tumor promoting stage in skin tumorigenesis by modulating multiple gene and protein in cancer signaling pathways without apparent toxicity.

Matched MeSH terms: Carcinogens/toxicity
Fulltext An Electrochemical DNA Biosensor for Carcinogenicity of Anticancer Compounds Based on Competition between Methylene Blue and Oligonucleotides

Md Sani ND, Ariffin EY, Sheryn W, Shamsuddin MA, Heng LY, Latip J, et al.

Sensors (Basel), 2019 Nov 22;19(23).
PMID: 31766637 DOI: 10.3390/s19235111

A toxicity electrochemical DNA biosensor has been constructed for the detection of carcinogens using 24 base guanine DNA rich single stranded DNA, and methylene blue (MB) as the electroactive indicator. This amine terminated ssDNA was immobilized onto silica nanospheres and deposited on gold nanoparticle modified carbon-paste screen printed electrodes (SPEs). The modified SPE was initially exposed to a carcinogen, followed by immersion in methylene blue for an optimized duration. The biosensor response was measured using differential pulse voltammetry. The performance of the biosensor was identified on several anti-cancer compounds. The toxicity DNA biosensor demonstrated a linear response range to the cadmium chloride from 0.0005 ppm to 0.01 ppm (R2 = 0.928) with a limit of detection at 0.0004 ppm. The biosensor also exhibited its versatility to screen the carcinogenicity of potential anti-cancer compounds.

Matched MeSH terms: Carcinogens/chemistry*
Daily exposure to toxic metals through urban road dust from industrial, commercial, heavy traffic, and residential areas in Petaling Jaya, Malaysia: a health risk assessment

Shabanda IS, Koki IB, Low KH, Zain SM, Khor SM, Abu Bakar NK

Environ Sci Pollut Res Int, 2019 Dec;26(36):37193-37211.
PMID: 31745807 DOI: 10.1007/s11356-019-06718-2

Human health is threatened by significant emissions of heavy metals into the urban environment due to various activities. Various studies describing health risk analyses on soil and dust have been conducted previously. However, there are limited studies that have been carried out regarding the potential health risk assessment of heavy metals in urban road dust of < 63-μm diameter, via incidental ingestion, dermal contact, and inhalation exposure routes by children and adults in developing countries. Therefore, this study evaluated the health risks of heavy metal exposure via ingestion, dermal contact, and inhalation of urban dust particles in Petaling Jaya, Malaysia. Heavy metals such as lead (Pb), chromium (Cr), zinc (Zn), copper (Cu), and manganese (Mn) were measured using dust samples obtained from industrial, high-traffic, commercial, and residential areas by using inductively coupled plasma mass spectrometry (ICP-MS). The principal component and hierarchical cluster analysis showed the dominance of these metal concentrations at sites associated with anthropogenic activities. This was suggestive of industrial, traffic emissions, atmospheric depositions, and wind as the significant contributors towards urban dust contamination in the study sites. Further exploratory analysis underlined Cr, Pb, Cu, and Zn as the most representative metals in the dust samples. In accommodating the uncertainties associated with health risk calculations and simulating the reasonable maximum exposure of these metals, the related health risks were estimated at the 75th and 95th percentiles. Furthermore, assessing the exposure to carcinogenic and non-carcinogenic metals in the dust revealed that ingestion was the primary route of consumption. Children who ingested dust particles in Petaling Jaya could be more vulnerable to carcinogenic and non-carcinogenic risks, but the exposure for both children and adults showed no potential health effects. Therefore, this study serves as an important premise for a review and reformation of the existing environmental quality standards for human health safety.

Matched MeSH terms: Carcinogens/analysis
Suppression of β-catenin and cyclooxygenase-2 expression and cell proliferation in azoxymethane-induced colonic cancer in rats by rice bran phytic acid (PA)

Saad N, Esa NM, Ithnin H

Asian Pac J Cancer Prev, 2013;14(5):3093-9.
PMID: 23803085

BACKGROUND: Phytic acid (PA) is a polyphosphorylated carbohydrate that can be found in high amounts in most cereals, legumes, nut oil, seeds and soy beans. It has been suggested to play a significant role in inhibition of colorectal cancer. This study was conducted to investigate expression changes of β-catenin and cyclooxygenase-2 (COX-2) and cell proliferation in the adenoma-carcinoma sequence after treatment with rice bran PA by immunocytochemistry.
MATERIALS AND METHODS: Seventy-two male Sprague-Dawley rats were divided into 6 equal groups with 12 rats in each group. For cancer induction two intraperitoneal injections of azoxymethane (AOM) were given at 15 mg/kg bodyweight over a 2-weeks period. During the post initiation phase, two different concentrations of PA, 0.2% (w/v) and 0.5% (w/v) were administered in the diet.
RESULTS: Results of β-catenin, COX-2 expressions and cell proliferation of Ki-67 showed a significant contribution in colonic cancer progression. For β-catenin and COX-2 expression, there was a significant difference between groups at p<0.05. With Ki-67, there was a statistically significant lowering the proliferating index as compared to AOM alone (p<0.05). A significant positive correlation (p=0.01) was noted between COX-2 expression and proliferation. Total β-catenin also demonstrated a significant positive linear relationship with total COX-2 (p=0.044).
CONCLUSIONS: This study indicated potential value of PA extracted from rice bran in reducing colonic cancer risk in rats.

Matched MeSH terms: Carcinogens/toxicity
Isolation of a quinone-rich fraction from Ardisia crispa roots and its attenuating effects on murine skin tumorigenesis

Yeong LT, Hamid RA, Yazan LS, Khaza'ai H

Asian Pac J Cancer Prev, 2013;14(4):2301-5.
PMID: 23725131

Ardisia crispa (Family: Myrsinaceae) is an evergreen, fruiting shrub that has been traditionally used as folklore medicine. Despite a scarcity of research publications, we have succeeded in showing suppressive effects on murine skin papillomagenesis. In extension, the present research was aimed at determining the effect of a quinone-rich fraction (QRF) isolated from the same root hexane extract on both initiation and promotion stages of carcinogenesis, at the selected dose of 30 mg/kg. Mice (groups I-IV) were initiated with a single dose of 7,12-dimethylbenz(α)anthracene (DMBA, 100 μg/100 μl) followed by repeated promotion of croton oil (1%) twice weekly for 20 weeks. In addition, group I (anti-initiation) received QRF 7 days before and after DMBA; group II (anti-promotion) received QRF 30 minutes before each croton oil application; group III (anti-initiation/ promotion) was treated with QRF as a combination of group I and II. A further two groups served as vehicle control (group V) and treated control (group VI). As carcinogen control, group IV showed the highest tumor volume (8.79±5.44) and tumor burden (3.60±1.17). Comparatively, group III revealed only 20% of tumor incidence, tumor burden (3.00±1.00) and tumor volume (2.40±1.12), which were significantly different from group IV. Group II also showed significant reduction of tumor volume (3.11), tumor burden (3.00) and tumor incidence (11.11%), along with prominent increase of latency period of tumor formation (week 12). Group I, nonetheless, demonstrated marked increment of tumor incidence by 40% with prompted latency period of tumor formation (week 7). No tumor formation was observed in groups V and VI. This study provided clear evidence of inhibitory effects of QRF during promotion period which was in agreement with our previous findings. The mechanism(s) underlying such effects have yet to be elucidated.

Matched MeSH terms: Carcinogens/toxicity
Inhibitory effects of Tualang Honey on experimental breast cancer in rats: a preliminary study

Kadir EA, Sulaiman SA, Yahya NK, Othman NH

Asian Pac J Cancer Prev, 2013;14(4):2249-54.
PMID: 23725121

The study was conducted to determine the effect of Malaysian jungle Tualang Honey (TH) on development of breast cancer induced by the carcinogen 7,12-dimethylbenz(α)anthracene (DMBA) in rats. Forty nulliparous female Sprague-Dawley rats were given 80 mg/kg DMBA then randomly divided into four groups: Group 1 served as a Control while Groups 2, 3 and 4 received 0.2, 1.0 or 2.0 g/kg bodyweight/day of TH, respectively, for 150 days. Results showed that breast cancers in the TH-treated groups had slower size increment and smaller mean tumor size (≤ 2 cm3) compared to Controls (≤ 8 cm3). The number of cancers developing in TH-treated groups was also significantly fewer (P<0.05). Histological grading showed majority of TH-treated group cancers to be of grade 1 and 2 compared to grade 3 in controls. There was an increasing trend of apoptotic index (AI) seen in TH-treated groups with increasing dosage of Tualang Honey, however, the mean AI values of all TH-treated groups were not significantly different from the Control value (p>0.05). In conclusion, Tualang Honey exerted positive modulation effects on DMBA-induced breast cancers in rats in this preliminary study.

Matched MeSH terms: Carcinogens/toxicity
The effect of chemical treatment on reduction of aflatoxins and ochratoxin A in black and white pepper during washing

Jalili M, Jinap S, Son R

Food Addit Contam Part A Chem Anal Control Expo Risk Assess, 2011 Apr;28(4):485-93.
PMID: 21416415 DOI: 10.1080/19440049.2010.551300

The effect of 18 different chemicals, which included acidic compounds (sulfuric acid, chloridric acid, phosphoric acid, benzoic acid, citric acid, acetic acid), alkaline compounds (ammonia, sodium bicarbonate, sodium hydroxide, potassium hydroxide, calcium hydroxide), salts (acetate ammonium, sodium bisulfite, sodium hydrosulfite, sodium chloride, sodium sulfate) and oxidising agents (hydrogen peroxide, sodium hypochlorite), on the reduction of aflatoxins B(1), B(2), G(1) and G(2) and ochratoxin A (OTA) was investigated in black and white pepper. OTA and aflatoxins were determined using HPLC after immunoaffinity column clean-up. Almost all of the applied chemicals showed a significant degree of reduction on mycotoxins (p < 0.05). The lowest and highest reduction of aflatoxin B(1), which is the most dangerous aflatoxin, was 20.5% ± 2.7% using benzoic acid and 54.5% ± 2.7% using sodium hydroxide. There was no significant difference between black and white peppers (p < 0.05).

Matched MeSH terms: Carcinogens, Environmental/analysis
Suppression of DMBA/croton oil-induced mouse skin tumor promotion by Ardisia Crispa root hexane extract

Roslida A, Fezah O, Yeong LT

Asian Pac J Cancer Prev, 2011;12(3):665-9.
PMID: 21627361

Ardisia crispa (Family: Myrsinaceae) has been used as a traditional medicine for various ailments. Previous studies showed that Ardisia crispa possesses antimetastatic and anti-inflammatory properties. Nevertheless, research done on the plant is still limited. Therefore, the present study was designed to evaluate the suppression effect of Ardisia crispa root hexane (ACRH) extract on 7, 12-dimethylbenz (α) anthracene (DMBA)-induced mice skin tumor promotion in ICR mice with topical application twice weekly for 10 weeks. Results showed significant difference between treatment groups (mice treated with 30 mg/kg, 100 mg/kg and 300 mg/kg of ACRH extract; denoted as group I, II and III respectively) for tumor incidence and tumor burden (P<0.05). Significant reduction in tumor incidence (20%), tumor burden (1.5 ± 0.50), tumor volume (2.49 ± 1.70) and delayed latency period of tumor formation was observed in group I (30 mg/kg) in comparison to carcinogen control. This study indicates that ACRH extract could be a promising skin tumor promotion suppressing agent at a lower dosage (30 mg/kg). Further studies are required to elucidate the underlying mechanism(s) leading to this effect.

Matched MeSH terms: Carcinogens/toxicity
Gene expression profiling of p53(+/-) knockout and wild-type mice following diethylstilbestrol administration

Salleh MN, Ismail P, Abdullah AS, Taufiq-Yap YH, Carmichael P

IUBMB Life, 2004 Jul;56(7):409-16.
PMID: 15545218

Studies with clastogenic carcinogen diethylstilbestrol (DES) resulted in a broad of spectrum of toxic and carcinogenic effects in humans and rodents, but the cellular and molecular mechanism(s) by which it induces cancer is not clear. To identify putative genetic targets for p53 in vivo, we applied the cDNA macroarray gene expression profiles associated with apoptosis by comparing p53+/- knockout mice and wild-type mice on the kidney and uterus of female mice. p53+/- knockout mice and wild-type mice were treated with DES (500 micromole kg(-1)) or vehicle i.p once daily for 4 days. Total RNAs were obtained from kidney and uterus of both control and DES-treated. The signal intensities of individual gene spots on the membrane were quantified and normalized to the expression level of the GAPDH gene as an internal control. Our results demonstrated that 16 genes; bad, bax, bcl-2, bcl-w, bcl-x, caspase-3, caspase-7, caspase-8, c-myc, E124, GADD45, mdm2, NKkappab1, p53, p21, Rb and trail were up-regulated and six genes; caspase-1, caspase-2, DR5, E2F1, FasL and iNOS did not changed in response to DES treatment in wild-type mice compared to p53+/- knockout mice. Most genes are involved in cell cycle regulation, signal transduction, apoptosis, or transcription. The greatest changes were seen in bad, bcl-x, mdm2, p53 and p21 gene expression in wild-type mice compared to p53+/- knockout mice. In comparing p53 and p21 gene expression in wild-type mice and p53+/- knockout mice, there was an 4.4-fold vs. 1.8-fold; 8-fold vs. 5.2-fold for kidney and 16-fold vs. 5.5-fold; 2.1-fold vs. 8.3-fold for uterus samples increase in induction (respectively). RT-PCR and densitometric analysis was used to confirm the biggest changes of p21, p53 and bax genes. Using this approach, we have identified apoptosis associated genes regulated in response to DES and have revealed putative differences between the isogenic parent strain and p53+/- knockout mice, which will contribute to a better understanding of toxicity/carcinogenicity mechanisms in this model.

Matched MeSH terms: Carcinogens/toxicity*

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