Ls in DCA-exposed rats suggest that DCA perturbs anterior pituitary hormone synthesis and secretion.abFig. 5 Testis sections of rats treated with (a) ADE and DCA at 0.5g/l showing significant improvement of histological architecture with normal seminiferous and sertoli cells, and (b) those treated with ADE and DCA at 2g/l showing mild degenerative changes of seminiferous tubules, mild congestion and edema (H E, 100?Arem et al. BMC Pharmacology and Toxicology (2017) 18:Page 7 ofIn our previous studies [45, 46] we have shown that DCA induced oxidative stress in liver and renal tissues by affecting endogenous antioxidant defense enzymes and lipid peroxidation. In the same way, in this study, we found that DCA induced oxidative stress in testicular tissues illustrated by an alteration in antioxidant enzymes activity and in lipid peroxidation level beside a decrease in GSH level. Antioxidant enzymes represent a defense mechanism, and are responsible for detoxification of reactive oxygen species (ROS). The SOD AT system provides the first defense against oxygen toxicity. SOD is considered to be one of the most active enzymes, its activity is sufficient for the dismutation of superoxide anions to hydrogen peroxide (H2O2) produced during oxidative stress in cells [47]. The elimination of H2O2 is either effected by CAT or GPx, with the latter playing predominating role in the testes [48]. Induction of SOD could occur during high production of superoxide anion. Therefore, an increase in the SOD activity indicates an increase of O- production. Also, the elevated activity of 2 CAT may due to the adaptive response to the generated free radicals. Thus increased activities of SOD and CAT may serve as protective responses to eliminate reactive free radicals [49]. GPx is involved in catalyzing the reduction of H2O2 at the expense of reduced GSH [50]. The level of GPx in the DCA-intoxicated rats, namely those receiving the higher dose, was depleted which can be attributed to either increased H2O2 generation or decreased GSH concentration. Decrease in GSH level as observed in the present study may be due to increased utilization of GSH for metabolism of lipid hydroperoxides by GPx or interaction of GSH with free radicals [13]. Thiol-based antioxidant system is the primary line of defense against oxidative stress. The decreased concentration of GSH increases the sensitivity of organ to oxidative and chemical injury and is one of the primary factors which permit lipid peroxidation. In agreement with this hypothesis is the increase in MDA levels in rats’ testes observed in this study. MDA is a major oxidation product of peroxidized polyunsaturated fatty acids and increased MDA content is an important indicator of lipid peroxidation [51]. Therefore the increase in lipid peroxidation is the reflection of damage caused to the membranous structures. These disturbances in antioxidant enzyme and non-enzymatic systems and increases in lipid peroxidation in testes of rats intoxicated with DCA in the present study are in agreement with those induced by NSC309132 web different other environment toxicants [15, 52?5]. Histoarchitecture changes as seen in this study are supported by the significant changes seen in the enzymes and non-enzyme PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26240184 antioxidant defense systems as well as lipid peroxidation, which reflect increased ROS production. Nagda and Bhatt [13] suggested that enhancement of ROS production in thetestes may further damage vital components of the cell, like nucleic acids an.
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