ABSTRACT
Background and Aim: Sodium arsenite is an environmental pollutant with the capacity of generating free radicals and tissue damage. The aim of the current study was to investigate the effect of green tea extract [GTE], as an antioxidant, on sperm parameters and testis tissues of the mice treated with sodium arsenite
Materials and Methods: Twenty-four adult male NMRI mice with mean body weight 30 +/- 5g were randomly divided into 4 equal groups: control, sodium arsenite [5mg/kg/d.], GTE [100mg/kg/d.] and sodium arsenite+GTE. Oral treatments were performed as long as 34 days. At the end of treatments, body and left testis weight were recorded and the left caudal epididymis of each subject was cut under Ham's F10. Then, the released spermatozoa were used to analyze sperm parameters. Sperm chromatin quality was assessed by nuclear staining using acridine orange and aniline blue. The left testis of each mouse was used for histopathological observation. The serum malondialdehyde [MDA] level was measured as an index of lipid peroxidation. Finally, the obtained data was analyzed by means of one-was ANOVA at the significant level P<0.05
Results: A significant decrease in the number, motility, viability [P<0.001] and normal morphology of sperm [P<0.01] and also in mean diameter of seminiferous tubules, germinal epithelium thickness [P<0.001] were found in the mice treated with sodium arsenite compared to the controls. The mice treated with sodium arsenite revealed a significant increase in the mean diameter of seminiferous tubules lumen and MDA levels [P<0.001]. The above parameters were significantly compensated in the sodium arsenite+GTE group. Sodium arsenite had no effect on the body and testis weight, diameter of spermatogonial nucleus, sperm DNA integrity, and histone-protamine replacement
Conclusion: The results indicate that green tea extract can partially be useful in reducing sodium arsenite-induced toxicity
ABSTRACT
Sensory neurons in dorsal root ganglia [DRG] undergo apoptosis after peripheral nerve injury. The aim of this study was to investigate sensory neuron death and the mechanism involved in the death of these neurons in cultured DRG. In this experimental study, L5 DRG from adult mouse were dissected and incubated in culture medium for 24, 48, 72 and 96 hours. Freshly dissected and cultured DRG were then fixed and sectioned using a cryostat. Morphological and biochemical features of apoptosis were investigated using fluorescent staining [Propidium iodide and Hoechst 33342] and the terminal Deoxynucleotide transferase dUTP nick end labeling [TUNEL] method respectively. To study the role of caspases, general caspase inhibitor [Z-VAD.fmk, 100 microM] and immunohistochemistry for activated caspase-3 were used. After 24, 48, 72 and 96 hours in culture, sensory neurons not only displayed morphological features of apoptosis but also they appeared TUNEL positive. The application of Z-VAD.fmk inhibited apoptosis in these neurons over the same time period. In addition, intense activated caspase-3 immunoreactivity was found both in the cytoplasm and the nuclei of these neurons after 24 and 48 hours. Results of the present study show caspase-dependent apoptosis in the sensory neurons of cultured DRG from adult mouse