Protective Effect of L-cysteine Against Sodium Valproate-induced Oxidant Injury in Testis of Rats

2019 ◽  
Vol 15 (2) ◽  
pp. 248-256 ◽  
Author(s):  
Fawziah A. Al-Salm ◽  
Rasha Al-Eisa ◽  
Reham Z. Hamza ◽  
Howayda E. Khaled ◽  
Nahla S. El-Shen
2020 ◽  
Vol 170 (2) ◽  
pp. 211-214
Author(s):  
L. V. Okhremchuk ◽  
I. Zh. Seminskii ◽  
M. A. Darenskaya ◽  
L. A. Grebenkina ◽  
L. I. Kolesnikova ◽  
...  

1985 ◽  
Vol 37 (9) ◽  
pp. 675-677 ◽  
Author(s):  
F. J. Miñano ◽  
J. S. Serrano ◽  
J. A. Durán ◽  
M. Sancibrián

2017 ◽  
Vol 36 (11) ◽  
pp. 1212-1221 ◽  
Author(s):  
RZ Hamza ◽  
NS El-Shenawy

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.


1998 ◽  
Vol 274 (1) ◽  
pp. H35-H42 ◽  
Author(s):  
Lois F. Richard ◽  
Thomas E. Dahms ◽  
Robert O. Webster

Adenosine is thought to prevent or reduce the increase in permeability, which is a hallmark of oxidant injury to endothelium. However, the effect of adenosine on endothelial cells directly exposed to oxidant species has not been demonstrated in vitro. By measuring the passage of Evan’s blue dye-labeled albumin across confluent monolayers, we demonstrated the ability of adenosine (0.1–100 μM) to lower basal permeability of human umbilical vein endothelial cells in a concentration-dependent fashion and prevent the permeability increase induced by exposure of the cells to xanthine plus xanthine oxidase (X/XO). Whereas pretreatment of monolayers for 10 min with adenosine (10 and 100 μM) prevented the X/XO-induced permeability increase, these same concentrations of adenosine failed to increase intracellular adenosine 3′,5′-cyclic monophosphate in X/XO-exposed cells. The protective effect of adenosine on endothelial monolayers was mimicked by adenosine amine congener and 5′-( N-ethylcarboxamido)adenosine but not by other agonists examined. Hence, the protective effect of adenosine against oxidant injury may include an adenosine 3′,5′-cyclic monophosphate-independent mechanism by direct action of adenosine at A1receptors on endothelial cells.


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