Displaying publications 1 - 20 of 69 in total

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  1. Cui T, Lu R, Liu C, Wu Z, Jiang X, Liu Y, et al.
    Sci Total Environ, 2024 May 20;926:171829.
    PMID: 38537812 DOI: 10.1016/j.scitotenv.2024.171829
    In recent years, the use of electronic vaping products (also named e-cigarettes) has increased due to their appealing flavors and nicotine delivery without the combustion of tobacco. Although the hazardous substances emitted by e-cigarettes are largely found to be much lower than combustible cigarettes, second-hand exposure to e-cigarette aerosols is not completely benign for bystanders. This work reviewed and synthesized findings on the second-hand exposure of aerosols from e-cigarettes and compared the results with those of the combustible cigarettes. In this review, different results were integrated based upon sampling locations such as residences, vehicles, offices, public places, and experimental exposure chambers. In addition, the factors that influence the second-hand exposure levels were identified by objectively reviewing and integrating the impacts of combustible cigarettes and e-cigarettes on the environment. It is a challenge to compare the literature data directly to assess the effect of smoking/vaping on the indoor environment. The room volume, indoor air exchange rate, puffing duration, and puffing numbers should be considered, which are important factors in determining the degree of pollution. Therefore, it is necessary to calculate the "emission rate" to normalize the concentration of pollutants emitted under various experimental conditions and make the results comparable. This review aims to increase the awareness regarding the harmful effects of the second-hand exposure to aerosols coming from the use of cigarettes and e-cigarettes, identify knowledge gaps, and provide a scientific basis for future policy interventions with regard to the regulation of smoking and vaping.
    Matched MeSH terms: Nicotine
  2. Mohamed N, Muhammad N, Shuid AN, Soelaiman IN
    Curr Drug Targets, 2018;19(12):1424-1430.
    PMID: 28950810 DOI: 10.2174/1389450118666170925154428
    Nicotine is one of the most abused substances worldwide and can cause several harmful effects on health. One of the harmful effects, which is often ignored, is osteoporosis. Smoking has been shown to cause a decrease in bone mineral density in humans. Animal studies have proven that nicotine exerts negative effects on bone. The number of people who smoke increases each day. Those who smoke start at a very young age and they usually smoke for years. This will increase the risk of developing osteoporosis. As the prevalence of osteoporosis increases, the risk of fractures also increases. The major concerns are disability following fractures, mortality due to complications after fractures and the increasing cost of management and therapy. This paper will review the effects of nicotine on bone and the potential natural products which can be used as treatment for nicotine-induced osteoporosis.
    Matched MeSH terms: Nicotine/adverse effects*
  3. Man CN, Gam LH, Ismail S, Lajis R, Awang R
    PMID: 16908224
    Nicotine is a major addictive compound in cigarette. Its smoke is rapidly and extensively metabolized to several metabolites in human. Cotinine as a major metabolite of nicotine is commonly used as a biomarker to determine active and passive smokers. Cotinine has a longer half-life ( approximately 20 h) compared to nicotine ( approximately 2h). A simple, sensitive, rapid and high throughput GC-MS method was developed for simultaneous quantification of urinary nicotine and cotinine in passive and active smokers. In the sample preparation method, the analytes and internal standard were first basified and followed by liquid-liquid extraction. Upon completion, anhydrous sodium sulphate was added to the solvent mixture to trap moistures. The clear extract obtained was directly injected into GC-MS, operating under selective ion monitoring (SIM) mode. Calibration curves in the range of 0.5-5000 ng/mL of the analytes in urine matrix were established with linear correlation coefficients (r(2)) greater than 0.997. The limit of detection for both nicotine and cotinine were 0.20 ng/mL. The mean recoveries for nicotine and cotinine were 93.0 and 100.4%, respectively. The within- and between-assay accuracies were between 2.1 and 7.9% for nicotine and between 0.7 and 11.1% for cotinine. Within- and between-assay precisions of 3.3-9.5% for nicotine and 3.4-9.8% for cotinine were also achieved. The method can be used in routine assessment and monitoring of active smoking and exposure to environmental tobacco smoke. The applicability of the assay was demonstrated in a small-scale comparison study between smokers and non-smokers.
    Matched MeSH terms: Nicotine/urine*; Nicotine/chemistry
  4. Hapidin H, Othman F, Soelaiman IN, Shuid AN, Mohamed N
    Calcif. Tissue Int., 2011 Jan;88(1):41-7.
    PMID: 20953592 DOI: 10.1007/s00223-010-9426-4
    Nicotine is a major alkaloid of tobacco, which can increase free radical formation, leading to osteoporosis. The effects of nicotine administration and cessation on bone histomorphometry and biomarkers were studied in 28 Sprague-Dawley male rats. Rats aged 3 months and weighing 250-300 g were divided into four groups: control (C, normal saline for 4 months), nicotine for 2 months (N2), nicotine for 4 months (N4), and nicotine cessation (NC). The NC group was given nicotine for the first 2 months and then allowed to recover for the following 2 months without nicotine. Histomorphometric analysis was done using an image analyzer. ELISA kits were used to measure serum osteocalcin (bone formation marker) and pyridinoline (PYD, bone resorption marker) levels at month 0, month 2, and month 4. All test groups showed a significant decrease in BV/TV, Ob.S/BS, dLS/BS, MAR, BFR/BS, and osteocalcin levels and an increase in sLS/BS and PYD levels compared to group C. No significant differences were observed in all parameters measured among the test groups, except for MAR and BFR/BS. In conclusion, nicotine administration at a dose of 7 mg/kg for 2 and 4 months has detrimental effects on bone metabolism. Nicotine administration at 7 mg/kg for 2 months is sufficient to produce significant effects on bone histomorphometric parameters and biomarkers. In addition, prolonging the treatment for another 2 months did not show any significant differences. Cessation of nicotine for 2 months did not reverse the effects.
    Matched MeSH terms: Nicotine/administration & dosage; Nicotine/adverse effects; Nicotine/pharmacology*
  5. Hamira Farahana Hamdan, Syahrir Zaini
    MyJurnal
    Majority people with schizophrenia who smoke cigarettes, tend to be heavy smokers than other psychiatric patients and general population. Nicotine is one of the main components of cigarettes that can produce nicotinic interactions with antipsychotic drugs. Nicotine can also alleviate psychotic symptoms of schizophrenia. Aim: The objective for this systematic review is to examine the effects of nicotine and nicotine-based products in the treatment of schizophrenia, in comparison with placebo, no treatment or antipsychotic medication. Results: All studies comparing nicotine or other related products as the only treatment or adjunctive treatment for schizophrenia patients excluding the animal studies and case studies are reviewed. The use of traditional or known as typical antipsychotics may cause the patients to smoke frequently while patients taking atypical antipsychotics may smoke less. Patients who smoke may metabolize antipsychotics faster than non-smoking patients. There is less report related to smoking cessation among the schizophrenia patients. Conclusion: Neurobiological and psychosocial factors reinforce the high use of nicotine by patients with schizophrenia. Prior to smoking cessation implementation, it is crucial to understand on the ways and reasons for schizophrenia patients to consume nicotine for self-medicate symptoms which may lead to the development of new treatments for schizophrenia and nicotine dependence.
    Matched MeSH terms: Nicotine
  6. Rahman AU, Mohamed MHN, Jamshed S, Mahmood S, Iftikhar Baig MA
    J Pharm Bioallied Sci, 2020 Nov;12(Suppl 2):S671-S675.
    PMID: 33828359 DOI: 10.4103/jpbs.JPBS_245_19
    Background: The Fagerstrom test for nicotine dependence (FTND) is the most widely used scale for assessing nicotine dependence on conventional tobacco cigarettes (TCGs). But the FTND does not evaluate the subject's nicotine dependence to electronic cigarette (EC).

    Objective: The aim of this study was to develop and assess an equivalent modified FTND scale that measures the nicotine dependency via EC.

    Materials and Methods: The investigator developed the equivalent modified FTND scale that scores identical to the original scale, that is, 0-10. The developed scale piloted among 15 EC single users, that is, use only EC verified by carbon monoxide (CO) level of <8ppm. The assessment of the scale was done among 69 EC single users and observed for 1 year to determine their nicotine status.

    Results: The modified scale revealed an acceptable Cronbach α value of 0.725. Further test-retest reliability of the scale showed a satisfactory Spearman's rank correlation coefficient value of 0.730 (P > 0.05). A 1-year observation showed that of 69 single users, 11 single users completely stopped nicotine intake, 24 remained as EC single users, 15 shifted to dual-use, and 19 relapsed to TCG. Surprisingly, the EC users who completely stopped nicotine intake after 1 year had a low average nicotine dependence value of 3 that was measured by the modified FTND scale at the baseline.

    Conclusion: The modified FTND scale precisely identifies the physical dependence to nicotine via EC. Therefore, as per this study results the modified FTND scale can be applied in any EC-related studies to assess nicotine dependency via EC.

    Matched MeSH terms: Nicotine
  7. Muthuraju, S., Abdullah, J.M.
    Orient Neuron Nexus, 2011;2(1):10-14.
    MyJurnal
    Neuronal cell death results from various circumstances such as hypoxia, ischemic and neurodegenerative diseases (NDs). In these events, the resulting modification of neurotransmitters, either excitatory or inhibitory, mediate much of the neuronal damage. However, this consequence depends upon their pre and post synaptic receptor activities which are the key mechanism for signal regulation. Among these, acetylcholine (ACh) is a well known neurotransmitter which is predominantly involved in neuroprotection as well as cognitive functions through its receptors activity, particularly the nicotinic subtypes. Several lines of evidence suggest that among these subtypes, a7 nicotinic acetylcholine receptor (a7nAChR) offers much promise for neuroprotective role in relation to the central nervous system (CNS) disorders like schizophrenia and Alzheimer's disease (AD). Several lines of evidence exist to show the potential mechanisms in which this nAChR subtype and its agonists such as nicotine, that trigger the a7nAChR-mediated suppression of neuronal cell death. This review focuses on the potential role of a7nAChR in neuroprotection by examining recent experimental data, both in vitro and in vivo, that argue for the neuroprotective role of a7nAChR in the CNS.
    Matched MeSH terms: Nicotine
  8. Gunasegar S, Himratul-Aznita WH
    FEMS Yeast Res., 2019 Mar 01;19(2).
    PMID: 30476044 DOI: 10.1093/femsyr/foy123
    Candida albicans ATCC 14053 and Candida parapsilosis ATCC 22019 hyphal-wall protein 1 (HWP1) are involved in hyphae formation and pathogenesis. The transcriptional agglutinin-like sequence 3 (ALS3) genes in both species are responsible for the development of biofilm and colonization on tooth surfaces. Therefore, we investigated the expression of HWP1 and ALS3 quantitatively in C. albicans and C. parapsilosis and examined the biofilm structure upon exposure to various nicotine concentrations. In vitro, biofilms of Candida species were developed directly on slides using the Lab-Tek Chamber Slide System and visualized by confocal laser scanning microscopy. Quantitative real-time polymerase chain reaction was used to measure HWP1 and ALS3 expression in C. albicans ATCC 14053 and C. parapsilosis ATCC 22019. The results indicated that nicotine multiplied the number of yeast cells and increased the extracellular polysaccharides of Candida species. We also found that 1-2 mg/mL nicotine could enhance the formation of biofilm. The findings also revealed that the expression of HWP1 and ALS3 in Candida species were increased as the nicotine concentration increased. Therefore, nicotine influences the biofilm development of oral-associated C. albicans ATCC 14053 and C. parapsilosis ATCC 22019.
    Matched MeSH terms: Nicotine
  9. Shroff SM, Sreeramareddy CT
    Subst Abuse Treat Prev Policy, 2024 Jan 25;19(1):11.
    PMID: 38273314 DOI: 10.1186/s13011-024-00592-z
    BACKGROUND: Marketing and sales of e-cigarettes are unregulated in Malaysia. We analyzed content displayed on e-cigarette retailer websites to identify marketing claims, promotional strategies, and product details in the year 2022.

    METHODS: We analyzed 30 Malaysia-based retailer websites using a mixed methods approach. Data were extracted as the frequency of occurrences of marketing claims, presence of regulatory information, product types, and flavors of e-juice as per a predefined codebook based on published literature. We also extracted textual details published on the websites about marketing claims, and slogans.

    RESULTS: Most retailer websites provided contact information and physical store addresses (83%) but only half had 'click through' age verification (57%) that seldom needed any identification proof for age (3%). Marketing claims were related to health (47%), smoking cessation (37%), and modernity/trend (37%) and none had health warnings. Promotional strategies were discounts (80%). starter kits (57%) and email subscriptions (53%). Product types displayed were rechargeable (97%) and disposable (87%) devices and e-liquids (90%) of an array of flavors (> 100). Nicotine presence, its concentration, and "nicotine is an addictive chemical" were displayed in 93%, 53%, and 23% of websites respectively.

    CONCLUSION: Surveillance of content displayed online on e-cigarette retailer websites and regulation of online marketing and sales should be implemented by the Ministry of Health, Malaysia. Such measures are needed to prevent access to, and initiation of e-cigarette use among the youth and adults who do not smoke.

    Matched MeSH terms: Nicotine
  10. Omotoso GO, Kadir RE, Sulaimon FA, Jaji-Sulaimon R, Gbadamosi IT
    Malays J Med Sci, 2018 Sep;25(5):35-47.
    PMID: 30914861 DOI: 10.21315/mjms2018.25.5.4
    Background and aim: This study aimed to determine the effect of gestational nicotine exposure before neurodevelopment on the morphology and histology of the prefrontal cortex (PFC) in rats.

    Methodology: Adult female Wistar rats were time-mated and grouped into three categories: (a) control-given 0.1 mL of normal saline, (b) low-dose nicotine-given 6.88 mg/ kg/d/0.05 mL, and (c) high-dose nicotine-given 13.76 mg/kg/d/0.1 mL in two divided doses. Treatment was given intraperitoneally from gestational days 2 to 6. On postnatal day 15 (P15), the pups were separated from their mothers, anaesthetised and sacrificed, followed by intracardial perfusion with 4% paraformaldehyde. PFC was excised from the brain and processed for tissue histology, histochemistry, and morphology of brain cells.

    Results: Gestational nicotine exposure during the first week of gestation in rats significantly reduced birth weights in nicotine-treated groups compared with control; it, however, accelerated body weights, altered neuronal morphology, and elevated astrocytic count significantly, while oligodendroglial count was slightly increased in the PFC of juvenile rats examined at P15.

    Conclusion: These alterations revealed that gestational nicotine exposure before the commencement of the cellular processes involved in brain development negatively affects neurodevelopment, and this could result in neurological dysfunctions in later life.

    Matched MeSH terms: Nicotine
  11. Jayakumar R, Kanthimathi MS
    Food Chem, 2012 Oct 01;134(3):1580-4.
    PMID: 25005983 DOI: 10.1016/j.foodchem.2012.03.101
    Spices are rich sources of antioxidants due to the presence of phenols and flavonoids. In this study, the DNA protecting activity and inhibition of nicotine-induced cancer cell migration of 9 spices were analysed. Murine fibroblasts (3T3-L1) and human breast cancer (MCF-7) cells were pre-treated with spice extracts and then exposed to H₂O₂ and nicotine. The comet assay was used to analyse the DNA damage. Among the 9 spices, ginger, at 50 μg/ml protected against 68% of DNA damage in 3T3-L1 cells. Caraway, cumin and fennel showed statistically significant (p<0.05) DNA protecting activity. Treatment of MCF-7 cells with nicotine induced cell migration, whereas pre-treatment with spices reduced this migration. Pepper, long pepper and ginger exhibited a high rate of inhibition of cell migration. The results of this study prove that spices protect DNA and inhibit cancer cell migration.
    Matched MeSH terms: Nicotine/adverse effects*
  12. Norazlina M, Maizatul-Neza J, Azarina A, Nazrun AS, Norliza M, Ima-Nirwana S
    Med J Malaysia, 2010 Mar;65(1):14-7.
    PMID: 21265240 MyJurnal
    Vitamin E is found to reverse the effects of nicotine on bone and this study aimed to determine its mechanism. Male Sprague Dawley rats were divided into four groups and treated for 3 months: Group 1 was the control group (RC). Groups 2 (N), 3 (N+TT) and 4 (N+ATF) received nicotine 7 mg/kg throughout the treatment period. In addition, groups 3 and 4 received tocotrienol 60 mg/kg and alpha-tocopherol 60 mg/kg respectively during months 2 and 3. Parameters measured were serum osteoprotegerin (OPG), serum receptor activator of nuclear factor kappa B ligand (RANKL), femoral and lumbar bone calcium content and body weight. Nicotine did not affect OPG or RANKL levels but reduced bone calcium content suggesting the calcium loss is not due to increase osteoclastogenesis. OPG was increased in N+ATF while RANKL was slightly increased in N+TT. Both vitamin E supplements restored bone calcium loss induced by nicotine. Nicotine impaired weight gain in all treatment groups starting week 4 however, N+TT group was comparable to RC from week 6 onwards. Bone protective effects of ATF, but not TT, may be partly due to inhibition of osteoclastogenesis.
    Matched MeSH terms: Nicotine/toxicity*
  13. Awaisu A, Samsudin S, Amir NA, Omar CG, Hashim MI, Mohamad MH, et al.
    PMID: 20492717 DOI: 10.1186/1471-2288-10-46
    The purpose of the linguistic validation of the Wisconsin Smoking Withdrawal Scale (WSWS) was to produce a translated version in Malay language which was "conceptually equivalent" to the original U.S. English version for use in clinical practice and research.
    Matched MeSH terms: Nicotine/adverse effects
  14. King B, Yong HH, Borland R, Omar M, Ahmad AA, Sirirassamee B, et al.
    Tob Control, 2010 Dec;19(6):444-50.
    PMID: 20852322 DOI: 10.1136/tc.2009.034256
    This study explored the extent to which Malaysian and Thai smokers believe "light" and menthol cigarettes are less harmful than "regular" cigarettes and the correlates of these beliefs.
    Matched MeSH terms: Nicotine/adverse effects*
  15. Hapidin H, Othman F, Soelaiman IN, Shuid AN, Luke DA, Mohamed N
    J. Bone Miner. Metab., 2007;25(2):93-8.
    PMID: 17323178
    The effects of nicotine administration on bone-resorbing cytokines, cotinine, and bone histomorphometric parameters were studied in 21 Sprague-Dawley male rats. Rats aged 3 months and weighing 250-300 g were divided into three groups. Group 1 was the baseline control (BC), which was killed without treatment. The other two groups were the control group (C) and the nicotine-treated group (N). The N group was treated with nicotine 7 mg/kg body weight and the C group was treated with normal saline only. Treatment was given by intraperitoneal injection for 6 days/week for 4 months. The rats were injected intraperitoneally with calcein 20 mg/kg body weight at day 9 and day 2 before they were killed. ELISA test kits were used to measure the serum interleukin-1 (IL-1), interleukin-6 (IL-6), and cotinine (a metabolite of nicotine) levels at the beginning of the study and upon completion of the study. Histomorphometric analysis was done on the metaphyseal region of the trabecular bone of the left femur by using an image analyzer. Biochemical analysis revealed that nicotine treatment for 4 months significantly increased the serum IL-1, IL-6, and cotinine levels as compared to pretreatment levels. In addition, the serum cotinine level was significantly higher in the N group than in the C group after 4 months treatment. Histomorphometric analysis showed that nicotine significantly decreased the trabecular bone volume (BV/TV), trabecular thickness (Tb.Th), double-labeled surface (dLS/BS), mineralizing surface (MS/BS), mineral appositional rate (MAR), and bone formation rate (BFR/BS), while causing an increase in the single-labeled surface (sLS/BS), osteoclast surface (Oc.S/BS), and eroded surface (ES/BS) as compared to the BC and C groups. In conclusion, treatment with nicotine 7 mg/kg for 4 months was detrimental to bone by causing an increase in the bone resorbing cytokines and cotinine levels. Nicotine also exerted negative effects on the dynamic trabecular histomorphometric parameters.
    Matched MeSH terms: Nicotine/pharmacology*
  16. Al-Obaidi MM, Al-Bayaty FH, Al Batran R, Ibrahim OE, Daher AM
    Curr Pharm Des, 2016;22(16):2403-10.
    PMID: 27139374
    OBJECTIVES: -To examine the effect of nicotine (Ni) on bone socket healing treated with Ellagic acid (EA) after tooth extraction in rat.

    MATERIALS AND METHODS: Thirty-Two Sprague Dawley (SD) male rats were divided into four groups. The group 1 was administrated with distilled water intragastrically and injected sterile saline subcutaneously. The group 2 was administrated with EA orally and injected with sterile saline subcutaneously. The groups 3 & 4 were subcutaneously exposed to Ni for 4 weeks twice daily before tooth extraction procedure, and maintained Ni injection until the animals were sacrificed. After one month Ni exposure, the group 4 was fed with EA while continuing Ni injection. All the groups were anesthetized, and the upper left incisor was extracted. Four rats from each group were sacrificed on 14(th) and 28(th) days. Tumour necrosis factor alpha (TNFα), Interleukin-1 beta (IL-1β) and Interleukin-6 (IL-6) were applied to assess in serum rat at 14th and 28(th) days. Superoxide dismutase (SOD) and Thiobarbituric acid reactive substances (TBRAS) levels were assessed to evaluate the antioxidant status and lipid peroxidation accordingly after tooth extraction in homogenized gingival maxilla tissue of rat at 14(th) and 28(th) days. The socket hard tissue was stained by eosin and hematoxylin (H&E); immunohistochemical technique was used to assess the healing process by Osteocalcin (OCN) and Alkaline Phosphatase (ALP) biomarkers.

    RESULTS: Ni-induced rats administered with EA compound (Group 4) dropped the elevated concentration of pro-inflammatory cytokines significantly when compared to Ni-induced rats (Group 3) (p<0.05). Ni-induced rats administrated with EA compound (Group 4) showed significant production of SOD and recession in TBRAS level when compared to Ni-induced rats (Group 3) (p<0.05). The immunohistochemistry analysis has revealed that OCN and ALP have presented stronger expression in Ni-induced rats treated with EA (Group 4), as against Ni-induced rats (Group 3).

    CONCLUSION: We have concluded that, Ni-induced rats, treated with EA have exerted positive effect on the trabecular bone formation after tooth extraction in nicotinic rats could be due to the antioxidant activity of EA which lead to upregulate of OCN and ALP proteins which are responsible for osteogenesis.

    Matched MeSH terms: Nicotine/pharmacology*
  17. Onuki M, Yokoyama K, Kimura K, Sato H, Nordin RB, Naing L, et al.
    J Occup Health, 2003 May;45(3):140-5.
    PMID: 14646288
    To assess dermal absorption of nicotine from tobacco leaves in relation to Green Tobacco Sickness (GTS), urinary cotinine concentrations were measured in 80 male tobacco-growing farmers and in 40 healthy males (controls) who did not handle wet tobacco leaves in Kelantan, Malaysia. Among non-smokers, urinary cotinine levels in farmers were significantly higher than those of controls; farmers with urinary cotinine of 50 ng/ml/m2 or above showed eye symptoms more frequently than those below this level (p<0.05). Farmers who did not wear protective equipment had subjective symptoms more frequently than those who used the equipment (p<0.05); some of these symptoms were seen more frequently in organophosphate (Tamaron) users than in non-users. As tobacco farmers evidence a risk of nicotine poisoning from tobacco leaves, assessment including GTS together with effects of pesticides will be necessary.
    Matched MeSH terms: Nicotine/poisoning*
  18. Wong LP, Mohd Salim SN, Alias H, Aghamohammadi N, Hoe VCW, Isahak M, et al.
    J Addict Nurs, 2020 6 4;31(2):102-109.
    PMID: 32487936 DOI: 10.1097/JAN.0000000000000335
    Electronic cigarettes (e-cigarettes) have rapidly increased in popularity within the last 2 years in Malaysia. The study aims to understand the association between e-cigarette use behaviors and salivary cotinine (a CYP2AA metabolite of nicotine) concentration to inform the development of future e-cigarette control policies. A convenience sample of saliva from 144 e-cigarette users was obtained between November and December 2015. The study participants used refill liquid containing between 0 and 12 mg/ml of nicotine. The overall median cotinine concentration of the study participants was 81.1 ng/ml (interquartile range = 8.5-195.8). Among the zero-nicotine and single e-cigarette users, the median cotinine level was 51.1 (interquartile range = 8.20-125.35) ng/ml. Factors significantly associated with a higher salivary cotinine concentration were dual use of e-cigarettes and tobacco cigarettes, regular and daily e-cigarette use, a longer duration of e-cigarette use, using a higher amount of e-liquid, and a shorter duration to finish a refill. Multivariate analysis revealed that e-cigarette use of 1-6 and 6-12 months (but not 1 month and below) was significantly associated with a higher cotinine concentration. Cotinine found in zero-nicotine e-liquids implies the importance of stringent regulatory governance for the consistency of labeled nicotine content of e-cigarette liquid in the market. Zero-nicotine e-cigarette users should also be informed of the likelihood of environmental exposure to tobacco smoke. Future studies conducted on larger samples are warranted to validate the association between duration of e-cigarette use and salivary cotinine concentration as well as to investigate underlying mechanisms.
    Matched MeSH terms: Nicotine/administration & dosage
  19. Rahman A, Nik Mohamed MH, Mahmood S
    J Pharm Pharm Sci, 2021;24:200-209.
    PMID: 33909555 DOI: 10.18433/jpps31243
    PURPOSE: Evidence for the complete nicotine cessation is inadequate among electronic cigarettes (ECs) single users (SUs, use only ECs), and dual users (DUs, use both ECs and conventional cigarettes (CCs). The primary aim of this study was to evaluate the nicotine cessation among SUs and DUs who used ECs over one year.

    METHODS: We observed 70 SUs and 148 DUs for 52 weeks and tested their exhaled carbon monoxide and saliva cotinine to confirm their complete nicotine cessation status through cotinine in saliva. Safety issues were to be identified through self-report. Smoking cessation, CCs reduction of ≥ 50%, and relapsed to CCs smoking and safety issues were also documented.

    RESULTS: The nicotine cessation rate was higher in SUs then DUs (15.9% vs. 6.8%; P = 0.048; 95% CI (2.328-0.902). A similar result for smoking cessation (34.8% SUs vs. 17.1% DUs; P = 0.005; 95% CI: 2.031-0.787), whereas CCs ≥ 50% reduction was 23.3% DUs vs 21.7% SUs (P = 0.863; 95% CI :1.020-0.964). Relapse to CC smoking was 47.3% in DUs versus 30.4% in SUs (P = 0.026; 95% CI: 1.555-0.757). The adverse effects reported were coughing and breathing problems, whereas craving smoking was documented as a major withdrawal symptom. Smoking-related diseases were also identified, five in DUs and two in SUs, during the one-year study period.

    CONCLUSIONS: Study showed SUs achieved higher complete nicotine and smoking cessation rates as compared to DUs. However, the rates of reduced CC use were not different between both the groups. No serious adverse effects related to the sole use of ECs were detected. However, the safety of the sole use of ECs in absolute terms needs to be further validated in different populations.

    Matched MeSH terms: Nicotine*
  20. Hamirah NK, Kamsani YS, Mohamed Nor Khan NA, Ab Rahim S, Rajikin MH
    Med Sci Monit Basic Res, 2017 Dec 08;23:373-379.
    PMID: 29217815
    BACKGROUND Cytoskeletal structures, in particular actin and tubulin, provide a fundamental framework in all cells, including embryos. The objective of this study was to evaluate the effects of nicotine, which is a source of oxidative stress, and subsequent supplementation with Tocotrienol-rich fraction (TRF) on actin and tubulin of 2- and 8-cell murine embryos. MATERIAL AND METHODS Thirty female Balb/C mice were divided into 4 groups: Group 1 received: subcutaneous (sc) injection of 0.9% NaCl; Group 2 received sc injection of 3.0 nicotine mg/kg bw/day; Group 3 received 3.0 sc injection of nicotine mg/kg bw/day +60 mg/kg bw/day TRF; and Group 4 received 60 sc injection of TRF mg/kg bw/day for 7 consecutive days. The animals were superovulated with 5 IU PMSG followed by 5 IU hCG 48 h later. Animals were cohabited with fertile males overnight and euthanized through cervical dislocation at 24 h post coitum. Embryos at the 2- and 8-cell stages were harvested, fixed, and stained to visualize actin and tubulin distributions by using CLSM. RESULTS Results showed that at 2-cell stage, actin intensities were significantly reduced in the nicotine group compared to that of the control group (p<0.001). In Group 3, the intensity of actin significantly increased compared to that of the nicotine group (p<0.001). At 8-cell stage, actin intensity of the nicotine group was significantly lower than that of the control group (p<0.001). The intensities of actin in Group 3 were increased compared to that of nicotine treatment alone (p<0.001). The same trend was seen in tubulin at 2- and 8-cell stages. Interestingly, both actin and tubulin structures in the TRF-treated groups were enhanced compared to the control. CONCLUSIONS This study suggests that TRF prevents the deleterious effects of nicotine on the cytoskeletal structures of 2- and 8-cell stages of pre-implantation mice embryos in vitro.
    Matched MeSH terms: Nicotine/metabolism*
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