Glutathione S-Transferase M1 and T1 Polymorphisms and Susceptibility to Oxidative Damage in Healthy Korean Smokers

2010 ◽  
Vol 56 (1) ◽  
pp. 52-58 ◽  
Author(s):  
Sun Hee Lee ◽  
Eunju Park ◽  
Yoo Kyoung Park
Keyword(s):  
Oxidative Damage ◽  
Glutathione S Transferase

Melatonin protects against cadmium-induced oxidative damage in different tissues of rat: a mechanistic insight

2019 ◽  
Vol 2 (2) ◽  
pp. 1-21 ◽  
Author(s):  
Elina Mitra ◽  
Bharati Bhattacharjee ◽  
Palash Kumar Pal ◽  
Arnab Kumar Ghosh ◽  
Sanatan Mishra ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Oxidative Damage ◽  
Protein Carbonyl ◽  
Environmental Pollutant ◽  
Glutathione S Transferase ◽  
Protein Carbonyl Content ◽  
Wide Range ◽  
Liver And Kidney ◽  
Nadh Cytochrome ◽  
Cd Exposure

Cadmium (Cd) is a notorious environmental pollutant known for its wide range of toxicities to organisms. Thus, the present study is designed to examine whether melatonin, a potent antioxidant, protects against Cd-induced oxidative damage in the heart, liver and kidney of rats. Cd treatment at a dose of 0.44 mg/kg for 15 days caused severe damage in all these organs. These included significantly increased activities of SGPT, SGOT, lactate dehydrogenase- 1 and 5 and ALP and levels of total lactate, creatinine, lipid peroxidation, protein carbonyl content and reduced glutathione while the activities of superoxide dismutases, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase along with mitochondrial pyruvate dehydrogenase, isocitrate dehydrogenase, α-keto glutarate dehydrogenase, succinate dehydrogenase, NADH-cytochrome-c-oxidoreductase and cytochrome-c-oxidase were significantly reduced by Cd. However, if melatonin was given orally 30 min before Cd injection, all these alterations induced by Cd were significantly preserved by melatonin. Histological observations also demonstrated that Cd exposure caused cellular lesions, promoting necrotic or apoptotic changes. Notably, all these changes were significantly protected by melatonin. The results suggest that melatonin is a beneficial molecule to ameliorate Cd-induced oxidative damage in the heart, liver and kidney tissues of rats with its powerful antioxidant capacity, heavy metal chelating activity and competition of binding sites with Cd to the GSH and catalase.

Chemoprotective Effects of Propolis on Aflatoxin B1-Induced Hepatotoxicity in Rats: Oxidative Damage and Hepatotoxicity by Modulating TP53, Oxidative Stress

2020 ◽  
Vol 17 (3) ◽  
pp. 191-199
Author(s):  
Seval Yilmaz ◽  
Fatih Mehmet Kandemir ◽  
Emre Kaya ◽  
Mustafa Ozkaraca
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Oxidative Damage ◽  
Aflatoxin B1 ◽  
Tp53 Gene ◽  
Control Group ◽  
Glutathione S Transferase ◽  
Gene Expressions ◽  
Cat Gene ◽  
Gst Activity

Objective: This study aimed to detect hepatic oxidative damage caused by aflatoxin B1 (AFB1), as well as to examine how propolis protects against hepatotoxic effects of AFB1. Method: Rats were split into four groups as control group, AFB1 group, propolis group, AFB1+ propolis group. Results: There was significant increase in malondialdehyde (MDA) level and tumor suppressor protein (TP53) gene expression, Glutathione (GSH) level, Catalase (CAT) activity, CAT gene expression decreased in AFB1 group in blood. MDA level and Glutathione-S-Transferase (GST) activity, GST and TP53 gene expressions increased in AFB1 group, whereas GSH level and CAT activity alongside CAT gene expression decreased in liver. AFB1+propolis group showed significant decrease in MDA level, GST activity, TP53 and GST gene expressions, GSH level and CAT activity and CAT gene expression increased in liver compared to AFB1 group. Conclusion: These results suggest that propolis may potentially be natural agent that prevents AFB1- induced oxidative stress and hepatotoxicity.

scholarly journals Effects of Desiccation on Metamorphic Climax in Bombina variegata: Changes in Levels and Patterns of Oxidative Stress Parameters

Animals ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 953
Author(s):  
Tamara G. Petrović ◽  
Ana Kijanović ◽  
Nataša Kolarov Kolarov Tomašević ◽  
Jelena P. Gavrić ◽  
Svetlana G. Despotović ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Antioxidant System ◽  
Water Availability ◽  
System Control ◽  
Glutathione S Transferase ◽  
Oxidative Stress Parameters ◽  
Metamorphic Climax ◽  
Bombina Variegata ◽  
Stress Parameters

In this paper, we examined how the oxidative status (antioxidant system and oxidative damage) of Bombina variegata larvae changed during the metamorphic climax (Gosner stages: 42—beginning, 44—middle and 46—end) and compared the patterns and levels of oxidative stress parameters between individuals developing under constant water availability (control) and those developing under decreasing water availability (desiccation group). Our results revealed that larvae developing under decreasing water availability exhibited increased oxidative damage in the middle and end stages. This was followed by lower levels of glutathione in stages 44 and 46, as well as lower values of catalase, glutathione peroxidase, glutathione S-transferase and sulfhydryl groups in stage 46 (all in relation to control animals). Comparison between stages 42, 44 and 46 within treatments showed that individuals in the last stage demonstrated the highest intensities of lipid oxidative damage in both the control and desiccation groups. As for the parameters of the antioxidant system, control individuals displayed greater variety in response to changes induced by metamorphic climax than individuals exposed to desiccation treatment. The overall decrease in water availability during development led to increased oxidative stress and modifications in the pattern of AOS response to changes induced by metamorphic climax in larvae of B. variegata.

Glutathione S-transferase polymorphisms A1, M1, P1 and T1 are associated with enhanced oxidative damage among hemodialysis patients

2012 ◽  
Vol 53 ◽  
pp. S208
Author(s):  
T. Simic⁎ ◽  
S. Suvakov ◽  
A. Savic-Radojevic ◽  
M. Pljesa-Ercegovac ◽  
T. Damjanovic ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Hemodialysis Patients ◽  
Glutathione S Transferase

Oxidative damage and antioxidants in cervical cancer

2020 ◽  
pp. ijgc-2020-001587
Author(s):  
Daciele Paola Preci ◽  
Angélica Almeida ◽  
Anne Liss Weiler ◽  
Maria Luiza Mukai Franciosi ◽  
Andréia Machado Cardoso
Keyword(s):  
Cervical Cancer ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Oxidative Damage ◽  
Cancer Progression ◽  
Reduced Glutathione ◽  
Reactive Oxygen ◽  
Enzymatic Antioxidants ◽  
Glutathione S Transferase ◽  
The Impact

The pathogenesis of cervical cancer is related to oxidative damage caused by persistent infection by one of the oncogenic types of human papillomavirus (HPV). This damage comes from oxidative stress, which is the imbalance caused by the increase in reactive oxygen and nitrogen species and impaired antioxidant mechanisms, promoting tumor progression through metabolic processes. The incorporation of HPV into the cellular genome leads to the expression of oncoproteins, which are associated with chronic inflammation and increased production of reactive oxygen species, oxidizing proteins, lipids and DNA. The increase in these parameters is related, in general, to the reduction of circulating levels of enzymatic antioxidants—superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase; and non-enzymatic antioxidants—reduced glutathione, coenzyme Q10 and vitamins A, C and E, according to tumor staging. In contrast, some enzymatic antioxidants suffer upregulation in the tumor tissue as a way of adapting to the oxidative environment generated by themselves, such as glutathione-S-transferase, reduced glutathione, glutathione peroxidase, superoxide dismutase 2, induced nitric oxide synthase, peroxiredoxins 1, 3 and 6, and thioredoxin reductase 2. The decrease in the expression and activity of certain circulatory antioxidants and increasing the redox status of the tumor cells are thus key to cervical carcinoma prognosis. In addition, vitamin deficit is considered a possible modifiable risk factor by supplementation, since the cellular functions can have a protective effect on the development of cervical cancer. In this review, we will discuss the impact of oxidative damage on cervical cancer progression, as well as the main oxidative markers and therapeutic potentialities of antioxidants.

scholarly journals Amelioration of Isoproterenol-Induced Oxidative Damage in Rat Myocardium byWithania somniferaLeaf Extract

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Md. Ibrahim Khalil ◽  
Istiyak Ahmmed ◽  
Romana Ahmed ◽  
E. M. Tanvir ◽  
Rizwana Afroz ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Troponin I ◽  
Protective Role ◽  
Lipid Profiles ◽  
Enzymatic Antioxidants ◽  
Marker Enzymes ◽  
Glutathione S Transferase ◽  
Myocardial Membrane ◽  
Endogenous Antioxidant

We investigated the protective role ofWithania somniferaleaf extract (WSLEt) on isoproterenol- (ISO-) induced myocardial infarction (MI) in rats. Subcutaneous injection of ISO (85 mg/kg body weight (b.w.)) administered to rats for two consecutive days caused a significant increase in cardiac troponin I (cTnI) levels and serum lipid profiles, as well as the activities of some marker enzymes. In addition to these diagnostic markers, there were increased levels of lipid peroxidation (LPO) and decreased activities of enzymatic antioxidants (superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GRx), and glutathione-S-transferase (GST)) in the myocardium. However, oral pretreatment (100 mg/kg b.w.) with WSLEt for 4 weeks elicited a significant cardioprotective activity by lowering the levels of cTnI, lipid profiles, and marker enzymes. The levels of LPO products were also significantly decreased. Elevated activities of antioxidant enzymes were also observed in rats pretreated with WSLEt. As further confirmed histopathologically, our findings strongly suggest that the cardioprotective effect of WSLEt on myocardium experiencing ISO-induced oxidative damage may be due to an augmentation of the endogenous antioxidant system and an inhibition of LPO in the myocardial membrane. We conclude that WSLEt confers some protection against oxidative damage in ISO-induced MI in rats.

scholarly journals Exogenous thiourea modulates antioxidant defence and glyoxalase systems in lentil genotypes under arsenic stress

2016 ◽  
Vol 2 ◽  
pp. 9 ◽  
Author(s):  
Dibyendu Talukdar
Keyword(s):  
Oxidative Damage ◽  
Antioxidant Defense ◽  
Imaging Study ◽  
Dry Weight ◽  
Crop Productivity ◽  
Mitigation Strategies ◽  
Grain Legume ◽  
Glutathione S Transferase ◽  
Study Results ◽  
Antioxidant Defense Enzymes

<p>Arsenic (As) is a wide-spread toxic and carcinogenic metalloid, affecting crop productivity worldwide. Lentil, an edible grain legume, is increasingly exposed to soil arsenic contamination. However, our understandings regarding mechanistic details and mitigation strategies against arsenic toxicity in edible legume are extremely poor. Main purpose of the present study was to investigate the As-effects and its mitigation by thiourea (TU), a sulfhydryl bioregulator, in lentil. Four widely grown lentil genotypes were grown in nutrient media, supplemented with 30 μM sodium arsenate (As), As + 6.5 mM TU and As + 13 mM TU, keeping an untreated control for 10 d. As severely affected plant dry weight by accumulating in shoots and roots. However, TU application sequestered As in crop roots and prevented up-ward translocation of As. TU coordinately modulated glyoxalase system I and II (Gly I and II) and ascorbate (AsA)-glutathione (GSH) redox, and antioxidant defense enzymes in both leaves and roots of four genotypes. Elevation of Gly system prevented toxic methyl glyoxal overaccumulation whereas stimulated AsA-GSH cycle enzymes and Glutathione s-transferase and catalase effectively scavenged H<sub>2</sub>O<sub>2</sub> and prevented reactive oxygen species (ROS) -mediated onset of oxidative damage in four genotypes, as was evident from ROS-imaging study. Results suggested exogenous TU stimulated the Gly and antioxidant defense in fine tune against As-induced oxidative damage in lentil genotypes.</p>

Farnesol prevents Fe-NTA-mediated renal oxidative stress and early tumour promotion markers in rats

2006 ◽  
Vol 25 (5) ◽  
pp. 235-242 ◽  
Author(s):  
Tamanna Jahangir ◽  
Tajdar Husain Khan ◽  
Lakshmi Prasad ◽  
Sarwat Sultana
Keyword(s):  
Body Weight ◽  
Oxidative Damage ◽  
Quinone Reductase ◽  
Decarboxylase Activity ◽  
Protective Effects ◽  
Glutathione S Transferase ◽  
Metabolizing Enzymes ◽  
Excess Iron ◽  
Tumour Promotion ◽  
Malondialdehyde Formation

Excess iron deposition in tissues leads to organ dysfunction and impairment. In this study, the protective effects of farnesol (FL), an isoprenoid, against Fe-NTA (9 mg iron/kg body weight i.p.)-induced oxidative damage and early tumour promotion markers are evaluated. The pretreatment of iron-intoxicated rats with 1% and 2%/kg body weight oral dose of FL for 7 consecutive days significantly reversed the iron-induced increase in H2O2 content (P <0.001), malondialdehyde formation, xanthine oxidase activity (P <0.001), ornithine decarboxylase activity (P <0.001) and 3[H]thymidine incorporation in renal DNA (P <0.005) with simultaneous significant depletion in serum toxicity markers blood urea nitrogen (BUN) and creatinine (P <0.001). Significant dose-dependent restoration was recorded in renal glutathione content, its dependent enzymes and other phase II metabolizing enzymes viz., catalase, glutathione-S-transferase and quinone reductase (P <0.001) with prophylactic treatment of FL. Present results support that FL markedly lowers the oxidative damage and appearance of tumour markers, which precludes its development as a chemopreventive tool.

scholarly journals Mitigation Effects of a Novel Herbal Medicine, Hepad, on Neuroinflammation, Neuroapoptosis, and Neuro-Oxidation

Molecules ◽  
2018 ◽  
Vol 23 (11) ◽  
pp. 2920 ◽  
Author(s):  
Da Song ◽  
Gyeong-Ji Kim ◽  
Kwon Lee ◽  
Jae Shin ◽  
Dong-Hee Kim ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Neurodegenerative Disorder ◽  
Herbal Medicines ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Glutathione S Transferase ◽  
Neuroprotective Effects ◽  
Extracellular Signal ◽  
Enhanced Expression ◽  
Factor Α ◽  
Oxide Synthase

Parkinson’s disease (PD), a common adult-onset neurodegenerative disorder with complex pathological mechanisms, is characterized by the degeneration of dopaminergic nigrostriatal neurons. The present study demonstrated that the herbal medicines Hepad 1 and 2 protected against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic neurotoxicity in C57BL/6 mice and SH-SY5Y cells. Hepad 1 and 2 remarkably alleviated the enhanced expression of pro-inflammatory cytokines (tumor necrosis factor-α, interleukin-6, inducible nitric oxide synthase, cyclooxygenase-2, macrophage-1, and phosphorylated iκB-α) and apoptotic signals (Bcl-2-associated X protein, caspase-3, and poly [ADP-ribose] polymerase-1). Additionally, Hepad reduced MPTP-induced oxidative damage by increasing the expression of anti-oxidant defense enzymes (superoxide dismutase and glutathione S-transferase) and downregulating the levels of nicotinamide adenine dinucleotide phosphate oxidase 4. This study also showed that the neuroprotective effects of Hepad include anti-inflammatory, anti-apoptotic, and anti-oxidative properties, in addition to activation of the protein kinase B, extracellular-signal-regulated kinase, and c-Jun N-terminal kinase signaling pathways. Furthermore, oral administration of Hepad 1 and 2 attenuated the death of tyrosine hydroxylase-positive substantia nigra neurons that was induced by 20 mg/kg MPTP. Therefore, our results suggest that Hepad 1 and 2 are useful for treating PD and other disorders associated with neuro-inflammatory, neuro-apoptotic, and neuro-oxidative damage.

Effects of diallyl tetrasulfide on cadmium-induced oxidative damage in the liver of rats

2007 ◽  
Vol 26 (6) ◽  
pp. 527-534 ◽  
Author(s):  
P. Murugavel ◽  
L. Pari
Keyword(s):  
Lipid Peroxidation ◽  
Body Weight ◽  
Oxidative Damage ◽  
Antioxidant Defense ◽  
Protective Efficacy ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Vital Role ◽  
Glutathione S Transferase ◽  
Glucose 6 Phosphate Dehydrogenase

The protective efficacy of diallyl tetrasulfide (DTS) from garlic on liver injury induced by cadmium (Cd) was investigated. In this study, Cd (3 mg/kg body weight) was administered subcutaneously for 3 weeks to induce toxicity. DTS was administered orally (10, 20 and 40 mg/kg body weight) for 3 weeks with subcutaneous (sc) injection of Cd. Cd-induced liver damage was evidenced from increased activities of serum hepatic enzymes, namely aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase, with significant elevation of lipid peroxidation indices (thiobarbituric acid reactive substances and hydroperoxides) and protein carbonyl groups in the liver. Rats subjected to Cd toxicity also showed a decline in the levels of total thiols, reduced glutathione (GSH), vitamin C and vitamin E, accompanied by an increased accumulation of Cd, and significantly decreased activities of superoxide dismutase, catalase (CAT), glutathione peroxidase, glutathione-S-transferase (GST), glutathione reductase, and glucose-6-phosphate dehydrogenase in the liver. Administration of DTS at 40 mg/kg body weight significantly normalised the activities of hepatic marker enzymes, compared to other doses of DTS (10 and 20 mg/kg body weight). In addition, DTS (40 mg/kg body weight) significantly reduced the accumulation of Cd and the level of lipid peroxidation, and restored the level of antioxidant defense in the liver. Histological studies also showed that administration of DTS to Cd-treated rats resulted in a marked improvement of hepatocytes morphology with mild portal inflammation. Our results suggest that DTS might play a vital role in protecting Cd-induced oxidative damage in the liver. Human & Experimental Toxicology(2007) 26, 527—534

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