Influence of conventional antiepileptic drugs on glutathione-S-transferase and lipid peroxidation in children with idiopathic epilepsy

We report the effect of cross-sex hormonal replacement on antioxidant enzymes from rat retroperitoneal fat adipocytes. Eight rats of each gender were assigned to each of the following groups: control groups were intact female or male (F and M, resp.). Experimental groups were ovariectomized F (OvxF), castrated M (CasM), OvxF plus testosterone (OvxF + T), and CasM plus estradiol (CasM + E2) groups. After sacrifice, retroperitoneal fat was dissected and processed for histology. Adipocytes were isolated and the following enzymatic activities were determined: Cu-Zn superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and glutathione reductase (GR). Also, glutathione (GSH) and lipid peroxidation (LPO) were measured. In OvxF, retroperitoneal fat increased and adipocytes were enlarged, while in CasM rats a decrease in retroperitoneal fat and small adipocytes are observed. The cross-sex hormonal replacement in F rats was associated with larger adipocytes and a further decreased activity of Cu-Zn SOD, CAT, GPx, GST, GR, and GSH, in addition to an increase in LPO. CasM + E2exhibited the opposite effects showing further activation antioxidant enzymes and decreases in LPO. In conclusion, E2deficiency favors an increase in retroperitoneal fat and large adipocytes. Cross-sex hormonal replacement in F rats aggravates the condition by inhibiting antioxidant enzymes.

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Biochemical effects of glyphosate based herbicide, Excel Mera 71 on enzyme activities of acetylcholinesterase (AChE), lipid peroxidation (LPO), catalase (CAT), glutathione-S-transferase (GST) and protein content on teleostean fishes

Ecotoxicology and Environmental Safety ◽

10.1016/j.ecoenv.2014.05.025 ◽

2014 ◽

Vol 107 ◽

pp. 120-125 ◽

Cited By ~ 56

Author(s):

Palas Samanta ◽

Sandipan Pal ◽

Aloke Kumar Mukherjee ◽

Apurba Ratan Ghosh

Keyword(s):

Lipid Peroxidation ◽

Protein Content ◽

Enzyme Activities ◽

Glutathione S Transferase ◽

Biochemical Effects ◽

Excel Mera 71

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Plasma homocysteine and aminothiol levels in idiopathic epilepsy patients receiving antiepileptic drugs

Turkish Journal of Biochemistry ◽

10.1515/tjb-2018-0218 ◽

2019 ◽

Vol 44 (5) ◽

pp. 661-666

Author(s):

Dilber Çoban Ramazan ◽

Ülker Anadol ◽

A. Destina Yalçın ◽

A. Süha Yalçın

Keyword(s):

Valproic Acid ◽

Folic Acid ◽

Vitamin B12 ◽

Antiepileptic Drug ◽

Antiepileptic Drugs ◽

Serum Vitamin ◽

Idiopathic Epilepsy ◽

Serum Folate ◽

Significant Difference ◽

Epileptic Patients

Abstract Objective Homocysteine is a sulfur containing amino acid that is formed during methionine metabolism. Patients under long-term antiepileptic drug treatment often have hyperhomocysteinemia. These patients have low levels of serum folate, vitamin B12 and vitamin B6, all of which are associated with homocysteine metabolism. We have investigated the effects of valproic acid and new generation antiepileptic drugs (lamotrigine and levetiracetam) on plasma levels of homocysteine and aminothiols as well as serum vitamin B12 and folic acid. Materials and methods Forty-seven idiopathic epileptic patients on antiepileptic drugs were compared with 38 age-matched healthy controls. Commercial immunoassay methods were used for vitamin B12 and folic acid analyses. Homocysteine, cysteine, cysteinylglycine and glutathione levels were determined by high performance liquid chromatography. Results There was no significant difference in patient and control values in terms of vitamin B12, folic acid and homocysteine. Valproic acid and lamotrigine seemed to effect aminothiol redox status. Glutathione levels of epileptic patients receiving valproic acid and lamotrigine were higher than controls. Conclusion Our results suggest that redox homeostasis may be impaired and glutathione synthesis increased in response to the oxidative stress caused by antiepileptic drug use.

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Cellular Response to the Redox Active Lipid Peroxidation Products: Induction of Glutathione S-Transferase P by 4-Hydroxy-2-nonenal

Biochemical and Biophysical Research Communications ◽

10.1006/bbrc.1997.6585 ◽

1997 ◽

Vol 236 (2) ◽

pp. 505-509 ◽

Cited By ~ 61

Author(s):

Aya Fukuda ◽

Yoshimasa Nakamura ◽

Hajime Ohigashi ◽

Toshihiko Osawa ◽

Koji Uchida

Keyword(s):

Lipid Peroxidation ◽

Cellular Response ◽

Glutathione S Transferase ◽

Lipid Peroxidation Products ◽

Redox Active

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Salt stress-induced lipid peroxidation is reduced by glutathione S-transferase, but this reduction of lipid peroxides is not enough for a recovery of root growth in Arabidopsis

Plant Science ◽

10.1016/j.plantsci.2005.03.030 ◽

2005 ◽

Vol 169 (2) ◽

pp. 369-373 ◽

Cited By ~ 73

Author(s):

Maki Katsuhara ◽

Takeshi Otsuka ◽

Bunichi Ezaki

Keyword(s):

Lipid Peroxidation ◽

Salt Stress ◽

Root Growth ◽

Lipid Peroxides ◽

Glutathione S Transferase

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Lycopene modulates cholinergic dysfunction, Bcl-2/Bax balance, and antioxidant enzymes gene transcripts in monosodium glutamate (E621) induced neurotoxicity in a rat model

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2015-0388 ◽

2016 ◽

Vol 94 (4) ◽

pp. 394-401 ◽

Cited By ~ 20

Author(s):

Kadry Sadek ◽

Tarek Abouzed ◽

Sherif Nasr

Keyword(s):

Lipid Peroxidation ◽

Brain Tissue ◽

Creatine Phosphokinase ◽

Monosodium Glutamate ◽

Serum Cholinesterase ◽

Glutathione S Transferase ◽

Group Iii ◽

Group I ◽

Male Wistar Rats ◽

Induced Apoptosis

The effect of monosodium glutamate (MSG) on brain tissue and the relative ability of lycopene to avert these neurotoxic effects were investigated. Thirty-two male Wistar rats were distributed into 4 groups: group I, untreated (placebo); group II, injected with MSG (5 mg·kg−1) s.c.; group III, gastrogavaged with lycopene (10 mg·kg−1) p.o.; and group IV received MSG with lycopene with the same mentioned doses for 30 days. The results showed that MSG induced elevation in lipid peroxidation marker and perturbation in the antioxidant homeostasis and increased the levels of brain and serum cholinesterase (ChE), total creatine phosphokinase (CPK), creatine phosphokinase isoenzymes BB (CPK-BB), and lactate dehydrogenase (LDH). Glutathione S-transferase (GST), superoxide dismutase (SOD), and catalase (CAT) activities and gene expression were increased and glutathione content was reduced in the MSG-challenged rats, and these effects were ameliorated by lycopene. Furthermore, MSG induced apoptosis in brain tissues reflected in upregulation of pro-apoptotic Bax while lycopene upregulated the anti-apoptotic Bcl-2. Our results indicate that lycopene appears to be highly effective in relieving the toxic effects of MSG by inhibiting lipid peroxidation and inducing modifications in the activity of cholinesterase and antioxidant pathways. Interestingly, lycopene protects brain tissue by inhibiting apoptosis signaling induced by MSG.

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Protective effect of L-carnitine against cisplatin-induced liver and kidney oxidant injury in rats

Open Medicine ◽

10.2478/s11536-009-0021-x ◽

2009 ◽

Vol 4 (2) ◽

pp. 184-191 ◽

Cited By ~ 8

Author(s):

Kerim Cayir ◽

Ali Karadeniz ◽

Abdulkadir Yildirim ◽

Yildiray Kalkan ◽

Akar Karakoc ◽

...

Keyword(s):

Lipid Peroxidation ◽

Therapeutic Potential ◽

Protective Effects ◽

Sprague Dawley ◽

Glutathione S Transferase ◽

Kidney Dysfunction ◽

Degree Of Protection ◽

Sprague Dawley Rats ◽

Liver And Kidney ◽

Endogenous Antioxidants

AbstractThe present study was designed to investigate the protective effects of L-carnitine (LC) on changes in the levels of lipid peroxidation and endogenous antioxidants induced by cisplatin (cis-diamminedichloroplatinum II, CDDP) in the liver and kidney tissues of rats. Twenty-four Sprague Dawley rats were equally divided into four groups of six rats each: control, cisplatin, L-carnitine, and L-carnitine plus cisplatin. The degree of protection produced by L-carnitine was evaluated by determining the level of malondialdehyde (MDA). The activity of glutathione (GSH), glutathione peroxidase (GSH-Px), glutathione S-transferase (GST), and superoxide dismutase (SOD) were estimated from liver and kidney homogenates, and the liver and kidney were histologically examined as well. L-carnitine elicited significant liver and kidney protective activity by decreasing the level of lipid peroxidation (MDA) and elevating the activity of GSH, GSHPx, GST, and SOD. Furthermore, these biochemical observations were supported by histological findings. In conclusion, the present study indicates a significant role for reactive oxygen species (ROS) and their relation to liver and kidney dysfunction, and points to the therapeutic potential of LC in CDDP-induced liver and kidney toxicity.

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