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Potential chemoprevention activity of pterostilbene by enhancing the detoxifying enzymes in the HT-29 cell line

Harun Z, Ghazali AR

Asian Pac J Cancer Prev, 2012;13(12):6403-7.
PMID: 23464466

Detoxifying enzymes are present in most epithelial cells of the human gastrointestinal tract where they protect against xenobiotics which may cause cancer. Induction of examples such as glutathione S-transferase (GST) and its thiol conjugate, glutathione (GSH) as well as NAD(P)H: quinoneoxidoreductase (NQO1) facilitate the excretion of carcinogens and thus preventing colon carcinogenesis. Pterostilbene, an analogue of resveratrol, has demonstrated numerous pharmacological activities linked with chemoprevention. This study was conducted to investigate the potential of pterostilbene as a chemopreventive agent using the HT-29 colon cancer cell line to study the modulation of GST and NQO1 activities as well as the GSH level. Initially, our group, established the optimum dose of 24 hours pterostilbene treatment using MTT assays. Then, effects of pterostilbene (0-50 μM) on GST and NQO1 activity and GSH levels were determined using GST, NQO1 and Ellman assays, respectively. MTT assay of pterostilbene (0-100 μM) showed no cytotoxicity toward the HT-29 cell line. Treatment increased GST activity in the cell line significantly (p<0.05) at 12.5 and 25.0 μM. In addition, treatment at 50 μM increased the GSH level significantly (p<0.05). Pterostilbene also enhanced NQO1 activity significantly (p<0.05) at 12.5 μM and 50 μM. Hence, pterostilbene is a potential chemopreventive agent capable of modulation of detoxifiying enzyme levels in HT-29 cells.

Matched MeSH terms: Glutathione/metabolism; Glutathione Transferase/metabolism
Fulltext Oral supplementation of L-glutathione prevents ultraviolet B-induced melanogenesis and oxidative stress in BALB/c mice

Nagapan TS, Lim WN, Basri DF, Ghazali AR

Exp Anim, 2019 Nov 06;68(4):541-548.
PMID: 31243189 DOI: 10.1538/expanim.19-0017

Dietary antioxidant supplements such as L-glutathione have gained considerable attention in dermatology and cosmeceutical fields. L-glutathione possesses antiaging, antimelanogenic, antioxidant, and anticancer properties. This study aimed to investigate the inhibitory effects of L-glutathione on melanogenesis activity and oxidative stress in ultraviolet B (UVB)-irradiated BALB/c mice. Eighteen female BALB/c mice were randomly divided into 3 groups: a control group (n=6), a group without UVB irradiation and L-glutathione administration; a UVB irradiated group (n=6), a group irradiated with a UVB dose of 250 mJ/cm2 for 3 min; and a treatment group (n=6), a group irradiated with UVB and treated with 100 mg/kg of L-glutathione by oral gavage. Treatment was given for 14 days, and UVB irradiation was given on days 9, 11, and 13. Oral L-glutathione significantly (P<0.05) reduced lipid peroxidation and elevated superoxide dismutase activity the and glutathione level. L-glutathione also inhibited melanin content and tyrosinase activity significantly (P<0.05) as compared with the UVB-irradiated group. Histopathological examination also showed that L-glutathione reduced the deposition of melanin pigment in the basal layer of the epidermis as compared with that in UVB-irradiated mice. All in all, the present study demonstrated that L-glutathione has the potential to be developed as a photoprotection agent against UVB-induced oxidative stress and melanogenesis.

Matched MeSH terms: Glutathione/administration & dosage; Glutathione/pharmacology*
The endothelial nitric oxide synthase gene G894T, glutathione S-transferase (GSTM1 and GSTT1) polymorphisms as a risk factor in the patient with nephrolithiasis

Mehdi WA, Mehde AA, Yusof F, Raus RA, Resen AK, Ghazali H

Int J Biol Macromol, 2019 Nov 01;140:719-726.
PMID: 31445152 DOI: 10.1016/j.ijbiomac.2019.08.184

BACKGROUND: The genetic features indicate a crucial role in nephrolithiasis. The present study was aimed to investigate the role of Glutathione-S-transferase Mu (GSTM1), Glutathione-S- transferase Theta (GSTT1) and endothelial nitric oxide synthase (eNOs) gene polymorphism in nephrolithiasis.
METHODS: We involved a case-control study in which 480 individuals were divided into 240 healthy control and 240 patients with nephrolithiasis. For each patient and control, we measured biochemical criteria, levels of glutathione S-transferase, eNOs, GSTM1, GSTT1genes and eNOS genes polymorphism by PCR-RFLP.
RESULTS: GSTM1 and GSTT1 null genotypes are not a risk features for nephrolithiasis. The eNOS frequency GG, GT, and TT genotypes by using Ban II enzyme as restriction enzyme were found to be (48.33, 36.67, and 15.00) %. The eNOS frequency TT, GT, and GG genotypes by using the Ban II enzyme as restriction enzyme were found to be 15.84, 25.83, and 58.33%, respectively. The result showed an increase in serum eNOs levels were in the patient's group comparing to control.
CONCLUSIONS: This work is the first in the literature to study the relation between eNOs genes polymorphisms and nephrolithiasis. The results conclude that TT genotypes in the eNOs genes are associated with an increase the oxidative stress in patients.

Matched MeSH terms: Glutathione Transferase/genetics*
Oxidised low density lipoprotein causes human macrophage cell death through oxidant generation and inhibition of key catabolic enzymes

Katouah H, Chen A, Othman I, Gieseg SP

Int J Biochem Cell Biol, 2015 Oct;67:34-42.
PMID: 26255116 DOI: 10.1016/j.biocel.2015.08.001

Oxidised low density lipoprotein (oxLDL) is thought to be a significant contributor to the death of macrophage cells observed in advanced atherosclerotic plaques. Using human-derived U937 cells we have examined the effect of cytotoxic oxLDL on oxidative stress and cellular catabolism. Within 3h of the addition of oxLDL, there was a rapid, concentration dependent rise in cellular reactive oxygen species followed by the loss of cellular GSH, and the enzyme activity of both glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and aconitase. The loss of these catabolic enzymes was accompanied by the loss of cellular ATP and lower lactate generation. Addition of the macrophage antioxidant 7,8-dihydroneopterin inhibited the ROS generation, glutathione loss and catabolic inactivation. NOX was shown to be activated by oxLDL addition while apocynin inhibited the loss of GSH and cell viability. The data suggests that oxLDL triggers an excess of ROS production through NOX activation, and catabolic failure through thiol oxidation resulting in cell death.

Matched MeSH terms: Glutathione/antagonists & inhibitors; Glutathione/metabolism; Glutathione/agonists
Neuroprotective properties of Loranthus parasiticus aqueous fraction against oxidative stress-induced damage in NG108-15 cells

Wong DZ, Kadir HA, Lee CL, Goh BH

J Nat Med, 2012 Jul;66(3):544-51.
PMID: 22318341 DOI: 10.1007/s11418-011-0622-y

Loranthus parasiticus, a Chinese folk medicine, has been widely used for the treatment of brain diseases, particularly in southwest China. Hence, the present neuroprotection model was designed to investigate its neuroprotective properties against H(2)O(2)-induced oxidative stress in NG108-15 cells. L. parasiticus aqueous fraction (LPAF), which was selected in the present study, had proved to be the most active fraction among the other tested extracts and fractions in our previous screening. The restoration of depleted intracellular glutathione (GSH), a major endogenous antioxidant, by LPAF was observed after H(2)O(2) insult. Pretreatment with LPAF substantially reduced the production of intracellular reactive oxygen species generated from H(2)O(2). Apoptotic features such as externalization of phosphatidylserine and disruption of mitochondrial membrane potential were significantly attenuated by LPAF. In addition, cell cycle analysis revealed a prominent decrease in the H(2)O(2)-induced sub-G(1) population by LPAF. Moreover, apoptotic morphological analysis by DAPI nuclear staining demonstrated that NG108-15 cells treated with H(2)O(2) exhibited apoptotic features, while such changes were greatly reduced in cells pretreated with LPAF. Taken together, these findings confirmed that LPAF exerts marked neuroprotective activity, which raises the possibility of potential therapeutic application of LPAF for managing oxidative stress-related neurological disorders and supports the traditional use of L. parasiticus in treating brain-related diseases.

Matched MeSH terms: Glutathione/metabolism
Glutathione S transferase-theta (GSTT1) genetic polymorphism among Chinese, Malays and Indians in Singapore

Lee EJ, Wong JY, Yeoh PN, Gong NH

Pharmacogenetics, 1995 Oct;5(5):332-4.
PMID: 8563775

Glutathione S-transferase-theta (GSTT1) is subject to a genetic polymorphism where approximately 50% of a Caucasian population are homozygous for the null allele. Because of the possible association of the polymorphism with increased cancer risk in individuals, we genotyped by polymerase chain reaction 187 normal Chinese, 167 normal Malays and 152 normal Indians from Singapore and Malaysia. The proportion of Chinese, Malays and Indians with the null genotype were 58%, 38% and 16% respectively and mirrored previously reported frequencies of the GSTM1 null genotype in these populations. The frequency of the combined GSTM1 and GSTT1 null genotypes among Chinese, Malays and Indians were 37%, 22% and 5% respectively. The similarity with predicted frequencies indicated no interaction between the two genetic polymorphisms.

Matched MeSH terms: Glutathione Transferase/genetics*
Frequency of mutant CYP1A1, NAT2 and GSTM1 alleles in normal Indians and Malays

Zhao B, Lee EJ, Wong JY, Yeoh PN, Gong NH

Pharmacogenetics, 1995 Oct;5(5):275-80.
PMID: 8563767

Several xenobiotic metabolizing enzymes, including CYP1A1, NAT2 and GSTM1, are subject to genetic polymorphisms. Because these enzymes are important for the detoxification and/or bioactivation of drugs and carcinogens, these polymorphisms have important implications in therapeutics and cancer susceptibility. The distributions of CYP1A1, NAT2 and GSTM1 genotype frequencies in unrelated individuals of the Indian (n = 139) and Malay (n = 146) populations were characterized by the polymerase chain reaction. The respective allelic frequencies of wild-type and mutant alleles of CYP1A1 were 0.82 and 0.18 for the Indians, and 0.69 and 0.31 for the Malays. The frequencies of wild-type, M1, M2 and M3 of NAT2 among Indians were 0.44, 0.20, 0.32 and 0.04 respectively. The corresponding NAT2 allelic frequencies in Malays were 0.41, 0.12, 0.38 and 0.09. The GSTM1*A allele could not be amplified in 33.1% of Indians and 61.6% of Malays. At least one GSTM1*B allele was detected in 7.2% and 7.5% of the respective populations. The allelic frequencies of CYP1A1, NAT2 and GSTM1 among Malays are similar to previously reported frequencies among Chinese in the region. These findings will be of importance in the determination of cancer risks in these populations.

Matched MeSH terms: Glutathione Transferase/genetics*; Glutathione Transferase/metabolism
The selective cytotoxicity of the alkenyl glucosinolate hydrolysis products and their presence in Brassica vegetables

Kadir NH, David R, Rossiter JT, Gooderham NJ

Toxicology, 2015 Aug 6;334:59-71.
PMID: 26066520 DOI: 10.1016/j.tox.2015.06.002

Cruciferous vegetable consumption correlates with reduced risk of cancer. This chemopreventative activity may involve glucosinolates and their hydrolysis products. Glucosinolate-derived isothiocyanates have been studied for their toxicity and chemopreventative properties, but other hydrolysis products (epithionitriles and nitriles) have not been thoroughly examined. We report that these hydrolysis products differ in their cytotoxicity to human cells, with toxicity most strongly associated with isothiocyanates rather than epithionitriles and nitriles. We explored mechanisms of this differential cytotoxicity by examining the role of oxidative metabolism, oxidative stress, mitochondrial permeability, reduced glutathione levels, cell cycle arrest and apoptosis. 2-Propenylisothiocyanate and 3-butenylisothiocyanate both inhibited cytochome P450 1A (CYP1A) enzyme activity in CYP expressing MCL-5 cells at high cytotoxic doses. Incubation of MCL-5 cells with non-cytotoxic doses of 2-propenylisothiocyanate for 24h resulted in a dose-dependent inhibition of ethoxyresorufin O-deethylase, yet failed to affect CYP1A1 mRNA expression indicating interference with enzyme activity rather than inhibition of transcription. Increased reactive oxygen species (ROS) production was observed only for 2-propenylisothiocyanate treatment. 2-Propenylisothiocyanate treatment lowered reduced glutathione levels whereas no changes were noted with 3,4-epithiobutylnitrile. Cell cycle analysis showed that 2-propenylisothiocyanate induced a G2/M block whereas other hydrolysis products showed only marginal effects. We found that 2-propenylisothiocyanate and 3-butenylisothiocyanate induced cell death predominantly via necrosis whereas, 3,4-epithiobutylnitrile promoted both necrosis and apoptosis. Thus the activity of glucosinolate hydrolysis products includes cytotoxicity that is compound-class specific and may contribute to their putative chemoprotection properties.

Matched MeSH terms: Glutathione/metabolism
[FEATURES MANIFESTATIONS COMORBID CURRENTS OF GASTROESOPHAGEAL REFLUX DISEASE AND ARTERIAL HYPERTENSION DEPENDING ON THE DEGREE OF ARTERIAL HYPERTENSION]

Fadieienko G, Gridniev O

Georgian Med News, 2015 Nov.
PMID: 26656546

The purpose of research - to study the features of circadian profile of blood pressure (BP), the data of echocardiography, pH-monitoring, lipid spectrum, level of apelin and the state of the system "lipid peroxidation-antioxidant protection" in patients with a combination of arterial hypertension (AH) and gastroesophageal reflux disease (GERD) depending on the level of AH. It was examined 126 patients with combination of AH II stage, 2-3 degrees, and GERD, 70 (55.56%) men and 56 (44.44%) women, mean age 56.84 ± 1.17. The anthropometric indicators, a condition of "lipid peroxidation- antioxidant protection", the level of apelin, ambulatory blood pressure monitoring (ABPM), echocardiography, esophageal pH-monitoring were evaluated. Analysis of the results was performed using a computer program IBM SPSS Statistics 21.0 for Windows XP. According to the daily averages ABPM systolic BP/diastolic BP in the I group were 141.2 ± 0.8/90.4 ± 0.4 mm Hg., in II group - 163.3 ± 0.9/101.0 ± 0.5 mm Hg., in III group - 185.6 ± 0.8/112.1 ± 0.5 mm Hg., p = 0.001. There are only 25.39% of patients had normal indicators of the variability of BP among individuals with comorbidity. Transformation from mild AH to moderate was accompanied by a significant increase in the severity of left ventricular remodeling by type of concentric hypertrophy. The data of esophageal pH-monitoring allow us to classify the disorders as severe gastroesophageal reflux in patients with a combination of AH and GERD (DeMeester, 1993). In the group with first degree of AH the average rate of circulating apelin was 930.58 ± 56.27 pg/mL, for the patients with 2nd degree of AH - 880.56 ± 17.97 pg/ml, p>0.05, in patients with third degree of AH - 650.91 ± 12.87 pg/ml (p = 0.001). Assessment of lipid profile has allowed to establish the worse dyslipidemia in patients with 3rd degree of AH combined with GERD (atherogenic ratio - 3.11 ± 0.09). The deterioration of degree of AH combined with GERD accompanied by an increase of oxidative stress with increase of nitrites plasma and malondialdehyde concentration, and decrease of glutathione peroxidase and of SH-groups concentration. Increased degree of AH in patients with severe GERD accompanied by worsening of left ventricular remodeling, reduction of apelin levels, progression of dyslipidemia, and imbalances in the system of "lipid peroxidation-antioxidant protection."

Matched MeSH terms: Glutathione Peroxidase/blood
Fulltext Comparison of antioxidant effects of honey, glibenclamide, metformin, and their combinations in the kidneys of streptozotocin-induced diabetic rats

Erejuwa OO, Sulaiman SA, Wahab MS, Salam SK, Salleh MS, Gurtu S

Int J Mol Sci, 2011;12(1):829-43.
PMID: 21340016 DOI: 10.3390/ijms12010829

Hyperglycemia-induced increase in oxidative stress is implicated in diabetic complications. This study investigated the effect of metformin and/or glibenclamide in combination with honey on antioxidant enzymes and oxidative stress markers in the kidneys of streptozotocin (60 mg/kg; intraperitoneal)-induced diabetic rats. Diabetic rats were randomized into eight groups of five to seven rats and received distilled water (0.5 mL); honey (1.0 g/kg); metformin (100 mg/kg); metformin (100 mg/kg) and honey (1.0 g/kg); glibenclamide (0.6 mg/kg); glibenclamide (0.6 mg/kg) and honey (1.0 g/kg); metformin (100 mg/kg) and glibenclamide (0.6 mg/kg); or metformin (100 mg/kg), glibenclamide (0.6 mg/kg) and honey (1.0 g/kg) orally once daily for four weeks. Malondialdehyde (MDA) levels, glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities were significantly elevated while catalase (CAT) activity, total antioxidant status (TAS), reduced glutathione (GSH), and GSH:oxidized glutathione (GSSG) ratio was significantly reduced in the diabetic kidneys. CAT, glutathione reductase (GR), TAS, and GSH remained significantly reduced in the diabetic rats treated with metformin and/or glibenclamide. In contrast, metformin or glibenclamide combined with honey significantly increased CAT, GR, TAS, and GSH. These results suggest that combination of honey with metformin or glibenclamide might offer additional antioxidant effect to these drugs. This might reduce oxidative stress-mediated damage in diabetic kidneys.

Matched MeSH terms: Glutathione Peroxidase/metabolism; Glutathione Reductase/metabolism
Antioxidant protection of Malaysian tualang honey in pancreas of normal and streptozotocin-induced diabetic rats

Erejuwa OO, Sulaiman SA, Wahab MS, Sirajudeen KN, Salleh MS, Gurtu S

Ann Endocrinol (Paris), 2010 Sep;71(4):291-6.
PMID: 20398890 DOI: 10.1016/j.ando.2010.03.003

Glucotoxicity contributes to beta-cell dysfunction through oxidative stress. Our previous study demonstrated that tualang honey ameliorated renal oxidative stress and produced hypoglycemic effect in streptozotocin (STZ)-induced diabetic rats. This present study investigated the hypothesis that hypoglycemic effect of tualang honey might partly be due to protection of pancreas against oxidative stress. Diabetes was induced by a single dose of STZ (60 mg/kg; ip). Diabetic rats were randomly divided into two groups and administered distilled water (0.5 ml/d) and tualang honey (1.0 g/kg/d). Similarly, two groups of non-diabetic rats received distilled water (0.5 ml/d) and tualang honey (1.0 g/kg/d). The animals were treated orally for 28 days. At the end of the treatment period, the honey-treated diabetic rats had significantly (p<0.05) reduced blood glucose levels [8.8 (5.8)mmol/L; median (interquartile range)] compared with the diabetic control rats [17.9 (2.6)mmol/L]. The pancreas of diabetic control rats showed significantly increased levels of malondialdehyde (MDA) and up-regulation of superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities. Catalase (CAT) activity was significantly reduced while glutathione-S-transferase (GST) and glutathione reductase (GR) activities remained unchanged in the pancreas of diabetic rats. Tualang honey significantly (p<0.05) reduced elevated MDA levels. Honey treatment also restored SOD and CAT activities. These results suggest that hypoglycemic effect of tualang honey might be attributed to its antioxidative effect on the pancreas.

Matched MeSH terms: Glutathione Peroxidase/metabolism; Glutathione Reductase/analysis; Glutathione Reductase/metabolism; Glutathione Transferase/analysis; Glutathione Transferase/metabolism
Fulltext Differential responses to blood pressure and oxidative stress in streptozotocin-induced diabetic Wistar-Kyoto rats and spontaneously hypertensive rats: effects of antioxidant (honey) treatment

Erejuwa OO, Sulaiman SA, Wahab MS, Sirajudeen KN, Salleh MS, Gurtu S

Int J Mol Sci, 2011;12(3):1888-907.
PMID: 21673929 DOI: 10.3390/ijms12031888

Oxidative stress is implicated in the pathogenesis and/or complications of hypertension and/or diabetes mellitus. A combination of these disorders increases the risk of developing cardiovascular events. This study investigated the effects of streptozotocin (60 mg/kg; ip)-induced diabetes on blood pressure, oxidative stress and effects of honey on these parameters in the kidneys of streptozotocin-induced diabetic Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Diabetic WKY and SHR were randomized into four groups and received distilled water (0.5 mL) and honey (1.0 g/kg) orally once daily for three weeks. Control SHR had reduced malondialdehyde (MDA) and increased systolic blood pressure (SBP), catalase (CAT) activity, and total antioxidant status (TAS). SBP, activities of glutathione peroxidase (GPx) and glutathione reductase (GR) were elevated while TAS was reduced in diabetic WKY. In contrast, SBP, TAS, activities of GPx and GR were reduced in diabetic SHR. Antioxidant (honey) treatment further reduced SBP in diabetic SHR but not in diabetic WKY. It also increased TAS, GSH, reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio, activities of GPx and GR in diabetic SHR. These data suggest that differences in types, severity, and complications of diseases as well as strains may influence responses to blood pressure and oxidative stress.

Matched MeSH terms: Glutathione/metabolism
Modulation of C-reactive protein and tumour necrosis factor-α in collagen-induced arthritis in Dark Agouti rats: impact of collagen concentration on severity of arthritis

Tudave D, Radhakrishnan A, Chakravarthi S, Haleagrahara N

Inflamm Res, 2011 Oct;60(10):897-907.
PMID: 21633874 DOI: 10.1007/s00011-011-0349-y

OBJECTIVES: The study investigated the effect of collagen-induced arthritis in Dark Agouti (DA) rats on the level of C-reactive protein and inflammatory cytokine tumour necrosis factor-alpha (TNF-α).
SUBJECTS: Female Dark Agouti (DA) rats.
METHODS: Three different dosages of (2 mg/kg of body weight, 3 mg/kg of body weight and 4 mg/kg of body weight) collagen and complete Freund's adjuvant suspension were tested. After 45 days, serum C-reactive protein, TNF-α, superoxide dismutase and total glutathione assays were done. Radiographic and histopathological changes in the joints were compared.
RESULTS: All three groups showed signs of arthritic changes, confirmed by histopathological and radiographic changes. Severe arthritic changes were seen in the rats injected with 4 mg/kg of body weight of collagen. There was a significant increase in C-reactive protein, TNF-α, super oxide dismutase and total glutathione levels in the plasma in arthritis rats and the changes were more significant with 4 mg/kg of collagen.
CONCLUSION: These results demonstrated that the optimal dose to inject to experimental animals in order to get server arthritic changes was 4 mg/kg of collagen with complete Freund's adjuvant suspension. Severe arthritis changes induced significant elevation in plasma C-reactive protein and TNF-α levels.

Matched MeSH terms: Glutathione/metabolism
Fulltext Neuroprotective effects of alpha lipoic Acid on haloperidol-induced oxidative stress in the rat brain

Perera J, Tan JH, Jeevathayaparan S, Chakravarthi S, Haleagrahara N

Cell Biosci, 2011;1(1):12.
PMID: 21711768 DOI: 10.1186/2045-3701-1-12

Haloperidol is an antipsychotic drug that exerts its' antipsychotic effects by inhibiting dopaminergic neurons. Although the exact pathophysiology of haloperidol extrapyramidal symptoms are not known, the role of reactive oxygen species in inducing oxidative stress has been proposed as one of the mechanisms of prolonged haloperidol-induced neurotoxicity. In the present study, we evaluate the protective effect of alpha lipoic acid against haloperidol-induced oxidative stress in the rat brain. Sprague Dawley rats were divided into control, alpha lipoic acid alone (100 mg/kg p.o for 21 days), haloperidol alone (2 mg/kg i.p for 21 days), and haloperidol with alpha lipoic acid groups (for 21 days). Haloperidol treatment significantly decreased levels of the brain antioxidant enzymes super oxide dismutase and glutathione peroxidase and concurrent treatment with alpha lipoic acid significantly reversed the oxidative effects of haloperidol. Histopathological changes revealed significant haloperidol-induced damage in the cerebral cortex, internal capsule, and substantia nigra. Alpha lipoic acid significantly reduced this damage and there were very little neuronal atrophy. Areas of angiogenesis were also seen in the alpha lipoic acid-treated group. In conclusion, the study proves that alpha lipoic acid treatment significantly reduces haloperidol-induced neuronal damage.

Matched MeSH terms: Glutathione Peroxidase
Rutin, a bioflavonoid antioxidant protects rat pheochromocytoma (PC-12) cells against 6-hydroxydopamine (6-OHDA)-induced neurotoxicity

Magalingam KB, Radhakrishnan A, Haleagrahara N

Int J Mol Med, 2013 Jul;32(1):235-40.
PMID: 23670213 DOI: 10.3892/ijmm.2013.1375

Free radicals are widely known to be the major cause of human diseases such as neurodegenerative diseases, cancer, allergy and autoimmune diseases. Human cells are equipped with a powerful natural antioxidant enzyme network. However, antioxidants, particularly those originating from natural sources such as fruits and vegetables, are still considered essential. Rutin, a quercetin glycoside, has been proven to possess antioxidant potential. However, the neuroprotective effect of rutin in pheochromocytoma (PC-12) cells has not been studied extensively. Therefore, the present study was designed to establish the neuroprotective role of rutin as well as to elucidate the antioxidant mechanism of rutin in 6-hydroxydopamine (6-OHDA)-induced toxicity in PC-12 neuronal cells. PC-12 cells were pretreated with different concentrations of rutin for 4, 8 and 12 h and subsequently incubated with 6-OHDA for 24 h to induce oxidative stress. A significant cytoprotective activity was observed in rutin pretreated cells in a dose-dependent manner. Furthermore, there was marked activation of antioxidant enzymes including superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and total glutathione (GSH) in rutin pretreated cells compared to cells incubated with 6-OHDA alone. Rutin significantly reduced lipid peroxidation in 6-OHDA-induced PC-12 cells. On the basis of these observations, it was concluded that the bioflavonoid rutin inhibited 6-OHDA-induced neurotoxicity in PC-12 cells by improving antioxidant enzyme levels and inhibiting lipid peroxidation.

Matched MeSH terms: Glutathione/metabolism
Effect of γ-tocotrienol in counteracting oxidative stress and joint damage in collagen-induced arthritis in rats

Radhakrishnan A, Tudawe D, Chakravarthi S, Chiew GS, Haleagrahara N

Exp Ther Med, 2014 May;7(5):1408-1414.
PMID: 24940448

Tocotrienols exhibit a significant anti-inflammatory and antioxidant effect in numerous human diseases. However, the anti-inflammatory and antioxidant effects of tocotrienols in arthritic conditions are not well documented. Therefore, the effect of γ-tocotrienol supplementation against oxidative stress and joint pathology in collagen-induced arthritis in rats was investigated in the present study. Adult female Dark Agouti rats were randomly divided into groups: Control, γ-tocotrienol alone, arthritis alone and arthritis with γ-tocotrienol. Arthritis was induced using 4 mg/kg body weight collagen in complete Freund's adjuvant. The rats were treated orally with 5 mg/kg body weight of γ-tocotrienol between day 21 and day 45. After 45 days, serum C-reactive protein (CRP), tumor necrosis factor (TNF)-α, superoxide dismutase (SOD) and total glutathione (GSH) assays were conducted. γ-tocotrienol significantly reduced the arthritis-induced changes in body weight, CRP, TNF-α, SOD and the total GSH levels. There was a significant reduction in the arthritis-induced histopathological changes in the γ-tocotrienol treatment group. The data indicated that administration of γ-tocotrienol resulted in a significant antioxidant and anti-inflammatory effect on collagen-induced arthritis; therefore, γ-tocotrienol may have therapeutic potential as a long-term anti-arthritic agent in rheumatoid arthritis therapy.

Matched MeSH terms: Glutathione
The effect of zinc supplementation on antioxidant and lipid peroxidation status during Brachiaria decumbens intoxication in sheep

Zhang SS, Noordin MM, Rahman SO, Haron MJ

Vet Hum Toxicol, 2001 Apr;43(2):83-7.
PMID: 11308125

An attempt was made to clarify the association between zinc (Zn) and antioxidants due to Zn supplementation on lipid peroxidation occurring during Brachiaria decumbens intoxication. The concentration of Zn, copper, malondialdehyde (MDA), superoxide dismutase (SOD), and gluthathione peroxidase (GSH-Px) were determined in tissues. There was a gradual increment in the concentration of Zn and MDA in serum and hepatocytic SOD in groups given Zn + B decumbens. A decline in erythrocytic GSH-Px and SOD, and lower concentration of reduced glutathione in hepatocyte cytosols were also detected in these sheep. It is highly suggestive that Zn supplementation may depress antioxidant status and enhance lipid peroxidation during B decumbens intoxication.

Matched MeSH terms: Glutathione/blood; Glutathione/drug effects; Glutathione Peroxidase/blood; Glutathione Peroxidase/drug effects
Changes in hepatic phosphoprotein levels in mice infected with Plasmodium berghei

Maniam P, Zainal Abidin Abu Hassan, Noor Embi, Hasidah Mohd Sidek

Sains Malaysiana, 2012;41:721-729.

Hepatic phosphoprotein levels are altered in mouse liver as a manifestation of bacteria, virus or parasite infection. Identification of signaling pathways mediated by these hepatic proteins contribute to the current understanding of the mechanism of pathogenesis in malarial infection. The present study was undertaken to evaluate the changes in hepatic phosphoprotein levels during Plasmodium berghei infection. Our study revealed changes in levels of three hepatic phosphoproteins following P. berghei infection compared to non-infected controls. Peptide fragment sequence analysis using tandem mass spectrometry (MS/MS) showed these hepatic proteins to be homologs to haemoglobin beta (HBB), class
Pi glutathione S-tranferase (GSTPi) and carbonic anhydrase III (CAIII) proteins of Mus musculus species respectively from the NCBInr sequence database. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis predicted the involvement of these proteins in specific pathways in Mus musculus species; GSTPi in glutathione and drug metabolism and CAIII in nitrogen metabolism. This shows that P. berghei infection affects similar signaling pathways as those reported in other pathogenic infections such as that related to GSTPi and CAIII in response to oxidative stress.

Matched MeSH terms: Glutathione
Fulltext Blood haematology, serum thyroid hormones and glutathione peroxidase status in kacang goats fed inorganic iodine and selenium supplemented diets

Aghwan ZA, Sazili AQ, Alimon AR, Goh YM, Hilmi M

Asian-Australas J Anim Sci, 2013 Nov;26(11):1577-82.
PMID: 25049744 DOI: 10.5713/ajas.2013.13180

The effects of dietary supplementation of selenium (Se), iodine (I), and a combination of both on the blood haematology, serum free thyroxine (FT4) and free triiodothyronine (FT3) hormones and glutathione peroxidase enzyme (GSH-Px) activity were examined on twenty four (7 to 8 months old, 22±1.17 kg live weight) Kacang crossbred male goats. Animals were randomly assigned to four dietary treatments (6 animals in each group). Throughout 100 d of feeding trial, the animals of control group (CON) received a basal diet, while the other three groups were offered basal diet supplemented with 0.6 mg/kg diet DM Se (SS), or 0.6 mg/kg diet DM I (PI), or a combination of both Se and I, each at 0.6 mg/kg diet DM (SSPI). The haematological attributes which are haemoglobin (Hb), red blood cell (RBC), packed cell volume (PCV), mean cell volume (MCV), white blood cells (WBC), band neutrophils (B Neut), segmented neutrophils (S Neut), lymphocytes (Lymph), monocytes (Mono), eosinophils (Eosin) and basophils (Baso) were similar among the four treatment groups, while serum levels of Se and I increased significantly (p<0.05) in the supplemented groups. The combined dietary supplementation of Se and I (SSPI) significantly increased serum FT3 in the supplemented animals. Serum GSH-Px activity increased significantly in the animals of SS and SSPI groups. It is concluded that the dietary supplementation of inorganic Se and I at a level of 0.6 mg/kg DM increased serum Se and I concentration, FT3 hormone and GSH-Px activity of Kacang crossbred male goats.

Matched MeSH terms: Glutathione Peroxidase
Activation of Nrf2 signaling by sitagliptin and quercetin combination against β-amyloid induced Alzheimer's disease in rats

Li Y, Tian Q, Li Z, Dang M, Lin Y, Hou X

Drug Dev Res, 2019 09;80(6):837-845.
PMID: 31301179 DOI: 10.1002/ddr.21567

The objective of this study was to evaluate the neuroprotective effect of sitagliptin (Sita), quercetin (QCR) and its combination in β-amyloid (Aβ) induced Alzheimer's disease (AD). Male Sprague-Dawley rats, weighing between 220 and 280 g were used for experiment. Rats were divided into 5 groups (n = 10) and the groups were as follows: (a) Sham control; (b) Aβ injected; (c) Aβ injected + Sita 100; (d) Aβ injected + QCR 100; and (e) Aβ injected + Sita 100 + QCR 100. Cognitive performance was observed by the Morris water maze (MWM), biochemical markers, for example, MDA, SOD, CAT, GSH, Aβ1-42 level, Nrf2/HO-1 expression and histopathological study of rat brain were estimated. Pretreatment with Sita, QCR and their combination showed a significant increase in escape latency in particular MWM cognitive model. Further co-administration of sita and QCR significantly reduced Aβ1-42 level when compared with individual treatment. Biochemical markers, for example, increased SOD, CAT and GSH, decreased MDA were seen, and histopathological studies revealed the reversal of neuronal damage in the treatment group. Additionally, Nrf2/HO-1 pathway in rat's brain was significantly increased by Sita, QCR and their combination. Pretreatment with QCR potentiates the action of Sita in Aβ induced AD in rats. The improved cognitive memory could be because of the synergistic effect of the drugs by decreasing Aβ1-42 level, antioxidant activity and increased expression of Nrf2/HO-1 in rat brain.

Matched MeSH terms: Glutathione/metabolism

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