Oxidative stress may play a role in the DNA damage induced by acrylamide in spermatocytes.

<p>(A) The comet assay was conducted on spermatocytes treated with acrylamide (1 µM, 18 h) or glycidamide (0.5 µM, 18 h) in the presence or absence of hOGG1. Significant levels of DNA damage were not detected in the acrylamide treated spermatocytes in either the presence or absence of hOGG1. A modest but significant increase in Tail DNA % was observed in spermatocytes following glycidamide treatment in the absence of hOGG1 (<i>F</i>_7,677 = 134.4, *<i>p</i><0.001); however, hOGG1 treatment resulted in greater detection of Tail DNA % following glycidamide exposure. Treatment with H₂O₂ (500 µM, 5 min) was used as a positive control and produced significant increases in Tail DNA % in the presence of either enzyme (***<i>p</i><0.001). (B) Glutathione (GSH) levels in spermatocytes were measured using a GSH assay following acrylamide (1 µM, 18 h) or glycidamide exposure (0.5 µM, 18 h). No significant differences in GSH levels in male germ cells were observed following acrylamide or glycidamide treatment. Additionally, relatively low GSH levels were found in spermatocytes (0.19 µM) compared to P19 embryonal carcinoma cells (2.14 µM, <i>F</i>_3,6 = 1676.2, ***<i>p</i><0.001). Data are representative of n = 3 experiments (Average ±SEM).