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1.
Hum Exp Toxicol ; 36(11): 1212-1221, 2017 Nov.
Article in English | MEDLINE | ID: mdl-28988495

ABSTRACT

Oxidative stress caused by sodium valproate (SV) is known to play a key role in the pathogenesis of brain tissue. The present study was designed to evaluate the protective effect of l-cysteine (LC) on the antioxidants of brain tissue of rats. The animals were divided into six groups: control group 1 was treated with saline as vehicle, groups 2 and 3 were treated with low and high doses of SV (100 and 500 mg/kg, respectively), group 4 was treated with LC (100 mg/kg), and groups 5 and 6 were treated with low-dose SV + LC and high-dose SV + LC, respectively. All the groups were treated orally by gastric tube for 30 successive days. Some antioxidant parameters were determined. Brain tissue (cerebral cortex) of SV-treated animals showed an increase in lipid peroxidation (LPO) and reduction in activity of enzymatic antioxidant and total antioxidant levels. Histopathological examination of cerebral cortex of SV rats showed astrocytic swelling, inflammation, and necrosis. After 4 weeks of the combination treatment of SV and LC daily, results showed significant improvement in the activity of cathepsin marker enzymes and restored the structure of the brain. LC was able to ameliorate oxidative stress deficits observed in SV rats. LC decreased LPO level and was also able to restore the activity of antioxidant enzymes as well as structural deficits observed in the brain of SV animals. The protective effect of LC in SV-treated rats is mediated through attenuation of oxidative stress, suggesting a therapeutic role for LC in individuals treated with SV.


Subject(s)
Antioxidants/metabolism , Brain/drug effects , Cysteine/pharmacology , Oxidative Stress , Valproic Acid/toxicity , Animals , Anticonvulsants/adverse effects , Biomarkers , Brain/metabolism , Glutathione Peroxidase , Lipid Peroxidation , Male , Rats , Rats, Wistar , Superoxide Dismutase
2.
J Anim Physiol Anim Nutr (Berl) ; 96(1): 102-10, 2012 Feb.
Article in English | MEDLINE | ID: mdl-21288263

ABSTRACT

The present study was undertaken to evaluate the effects of feeding the male mice with miso that was prepared with a mixture of microbial starters on the level of lipid peroxidation as a marker of oxidative stress, antioxidant power of hepatocytes, the enzymatic and non-enzymatic antioxidant. The starters that were used in the preparation of miso were Aspergillus oryzae and Pleurotus ostreaus or A. oryzae and Bacillus subtilis. The miso that was prepared with A. oryzae and Bacillus subtilis has more effect on suppressing the oxidative stress and enhancement of endogenous antioxidant of hepatocytes and renal tissue of mice.


Subject(s)
Antioxidants/metabolism , Kidney/metabolism , Liver/metabolism , Soy Foods/analysis , Animal Feed , Animals , Diet/veterinary , Lipid Peroxidation , Male , Mice , Random Allocation
3.
Toxicol Lett ; 69(3): 249-56, 1993 Sep.
Article in English | MEDLINE | ID: mdl-8212065

ABSTRACT

An improved technique for the isolation of cardiac myocytes from adult rat is described. This method produced a high yield of isolated cardiomyocytes (30-35 x 10(6) cells/heart) with viability over 88%. The rod-shaped cells represented about 70% of the viable cardiac myocytes. The leakage of creatine phosphokinase (CPK) in the incubation medium from the control was about 37% at zero time. This model was used to investigate chloroform (CHCl3) cardiotoxicity by measuring dye exclusion, change the viable cardiac myocytes shape and CPK leakage. As a result of CHCl3 exposure, there was a significant decrease in Trypan blue exclusion after 30 min and during the entire time course. The percentage of rod-shaped cells decreased significantly during the whole period of the study. Also, a significant elevation in CPK leakage after treatment with 1000 ppm CHCl3 was observed. The data show that the present technique for cardiomyocytes isolation from adult rats produced high percentage of viable cells. Furthermore, the toxic effect of CHCl3 on cardiac myocytes was time dependent.


Subject(s)
Chloroform/toxicity , Heart/drug effects , Animals , Calcium/physiology , In Vitro Techniques , Male , Myocardium/pathology , Rats , Rats, Sprague-Dawley
4.
Toxicol Lett ; 69(1): 77-85, 1993 Jul.
Article in English | MEDLINE | ID: mdl-8356569

ABSTRACT

Chloroform (CHCl3) is widely used in the manufacture of drugs, cosmetics, plastics and cleaning agents. It is also found in chlorinated drinking water. This study was designed to investigate the toxic effect of CHCl3 on isolated male rat hepatocytes using several toxicity parameters. The hepatocytes were isolated by a collagenase perfusion technique and the cell viability was determined by Trypan blue exclusion. The leakage of cytosolic enzymes such as aspartate transaminase (AST) and alanine transaminase (ALT) after treatment with CHCl3 was measured. Reduced glutathione content (GSH) and its related enzymes, glutathione reductase (GSH-Rx) and glutathione peroxidase (GSH-Px), were also evaluated to study the effect of CHCl3 on hepatocytes. Exposure to 100 and 1000 ppm CHCl3 results in a significant decrease in cell after 30 min incubation. However, the effect of 1 and 10 ppm concentrations was observed at 60 min incubation. AST leakage was significantly increased in all treatment groups, while ALT was significantly increased at 100 and 1000 ppm CHCl3 after 60 and 30 min, respectively. As early as 15 min, GSH was decreased significantly at 1000 ppm, but at 100 and 10 ppm CHCl3 the decrease in GSH began after 30 and 120 min, respectively. GSH-Px activity did not changed. However, the activity of GSH-Rx was significantly decreased at 1000 ppm CHCl3 and at the same time GSH content was decreased. The data indicate that the toxic effect of CHCl3 was dose- and time-dependent. The degree of GSH depletion correlated with increased cytotoxicity and decreased GSH-Rx activity due to CHCl3.


Subject(s)
Chloroform/toxicity , Liver/drug effects , Alanine Transaminase/metabolism , Animals , Aspartate Aminotransferases/metabolism , Cell Survival/drug effects , Glutathione Peroxidase/metabolism , Glutathione Reductase/metabolism , Liver/enzymology , Male , Rats , Rats, Sprague-Dawley
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