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, 32 (4), 301-309

Evaluation of Some Biochemical Parameters and Brain Oxidative Stress in Experimental Rats Exposed Chronically to Silver Nitrate and the Protective Role of Vitamin E and Selenium

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Evaluation of Some Biochemical Parameters and Brain Oxidative Stress in Experimental Rats Exposed Chronically to Silver Nitrate and the Protective Role of Vitamin E and Selenium

Mouna Gueroui et al. Toxicol Res.

Abstract

Due to undesirable hazardous interactions with biological systems, this investigation was undertaken to evaluate the effect of chronic exposure to silver on certain biochemical and some oxidative stress parameters with histopathological examination of brain, as well as the possible protective role of selenium and/or vitamin E as nutritional supplements. Thirty six male rats were divided into six groups of six each: the first group used as a control group. Group II given both vitamin E (400 mg/kg) of diet and selenium (Se) (1 mg/L) in their drinking water. Group III given silver as silver nitrate (AgNO3) (20 mg/L). Group IV given vitamin E and AgNO3. Group V given both AgNO3 and selenium. Group VI given AgNO3, vitamin E and Se. The animals were in the same exposure conditions for 3 months. According to the results which have been obtained; there was an increase in serum lactate dehydrogenase (LDH), lipase activities and cholesterol level, a decrease in serum total protein, calcium and alkaline phosphatase (ALP) activity in Ag-intoxicated rats. Moreover, the findings showed that Ag+ ions affected antioxidant defense system by decreasing superoxide dismutase (SOD) activity and increasing vitamin E concentration with a high level of malondialdehyde (MDA) in brain tissue. The histological examination also exhibited some nervous tissue alterations including hemorrhage and cytoplasm vacuolization. However, the co-administration of selenium and/or vitamin E ameliorated the biochemical parameters and restored the histological alterations. In conclusion, this study indicated that silver could cause harmful effects in animal body and these effects can be more toxic in high concentrations or prolonged time exposure to this metal. However, selenium and vitamin E act as powerful antioxidants which may exercise adverse effect against the toxicity of this metal.

Keywords: Brain tissue; Oxidative stress; Rats; Selenium; Silver; Vitamin E.

Figures

Fig. 1
Fig. 1
Lipid peroxidation levels in brain tissue of control and experimental rats. **p < 0.01: significantly different from control group, #p<0.05, ##p < 0.01: significantly different from AgNO3.
Fig. 2
Fig. 2
Brain non-enzymatic antioxidant levels of control and experimental rats. (A) Reduced glutathione (GSH); (B) vitamin E. **p < 0.01: significantly different from control group, #p < 0.05: significantly different from AgNO3, +++p < 0.001: statistical difference between AgNO3+vit E, AgNO3+Se and AgNO3+vit E + Se.
Fig. 3
Fig. 3
Brain enzymatic antioxidant levels of control and experimental rats. (A) GSH-Px; (B) GST, C: GR. ##p < 0.01: statistical difference from AgNO3, +p<0.05, ++p < 0.01: statistical difference between AgNO3 +vit E, AgNO3 +Se and AgNO3 +vit E + Se.
Fig. 4
Fig. 4
Brain enzymatic antioxidant levels of control and experimental rats. (A) SOD, (B) CAT. *p < 0.05: significantly different from control group, #p < 0.05: statistical difference from AgNO3, +p < 0.05: statistical difference between AgNO3 +vit E, AgNO3 +Se and AgNO3 +vit E + Se.
Fig. 5
Fig. 5
Photographs showing histological changes in cerebral tissue in different groups; Control group (A); (Vit E + Se)-treated group (B), histological picture showed normal brain tissue; Ag-treated group (C) showed some abnormalities; nervous tissue exhibited hemorrhage, and vacuolated spaces in the affected area; (Ag + Vit E)-treated group (D), (Ag + Se)-treated group (E) and (Ag + Vit E + Se)-treated group (F) ameliorated brain tissue histological pictures with less vacuolated cytoplasm especially in vitamin E supplementation, histological damages significantly decreased. Optic microscopy section were stained using the haematoxylin-eosin method, 40×. neurons; glial cells; a net work of finely branching small blood vessels; hemorrhage; vacuolated cytoplasm.

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