BACKGROUND: This study was conducted for to explore the plausible pathway of Chenopodium album seed extract (CAE)-mediated sperm cell death. STUDY DESIGN: The role of CAE for its spermicidal action was assessed by (a) measuring lipid peroxidation, protein carbonyl content and intracellular glutathione content in CAE exposed sperm cells; (b) assaying antioxidant enzymes like catalase and superoxide dismutase (SOD); (c) analyzing protein expressions by using sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot analysis; (d) fluorimetric measurement of intracellular H(2)O(2) level and generation of reactive oxygen species (ROS) in CAE-treated sperm cells; and (e) DNA ladder formation study. RESULTS: CAE-induced sperm death is due to (a) lipid peroxidation of the sperm cell membrane, oxidation of some critical cellular proteins and depletion of intracellular reduced gluthathione, indicating production of ROS; (b) activation of Mn-SOD and inactivation of catalase favoring endogenous accumulation of H(2)O(2); (c) generation of O(2)(*-) at an enhanced rate during oxidative stress as evidenced by increased Mn-SOD activity and protein expression; (d) accumulation of ROS in spermatozoa reflected in the fluorimetric experiments; and (e) increased production of O(2)(*-) and H(2)O(2) induced apoptosis-like death in sperm cells as observed by DNA ladder formation. CONCLUSION: The sperm death mediated by CAE is due to oxidative damage of cellular macromolecules by in situ generation of ROS.
BACKGROUND: This study was conducted for to explore the plausible pathway of Chenopodium album seed extract (CAE)-mediated sperm cell death. STUDY DESIGN: The role of CAE for its spermicidal action was assessed by (a) measuring lipid peroxidation, protein carbonyl content and intracellular glutathione content in CAE exposed sperm cells; (b) assaying antioxidant enzymes like catalase and superoxide dismutase (SOD); (c) analyzing protein expressions by using sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot analysis; (d) fluorimetric measurement of intracellular H(2)O(2) level and generation of reactive oxygen species (ROS) in CAE-treated sperm cells; and (e) DNA ladder formation study. RESULTS: CAE-induced sperm death is due to (a) lipid peroxidation of the sperm cell membrane, oxidation of some critical cellular proteins and depletion of intracellular reduced gluthathione, indicating production of ROS; (b) activation of Mn-SOD and inactivation of catalase favoring endogenous accumulation of H(2)O(2); (c) generation of O(2)(*-) at an enhanced rate during oxidative stress as evidenced by increased Mn-SOD activity and protein expression; (d) accumulation of ROS in spermatozoa reflected in the fluorimetric experiments; and (e) increased production of O(2)(*-) and H(2)O(2) induced apoptosis-like death in sperm cells as observed by DNA ladder formation. CONCLUSION: The sperm death mediated by CAE is due to oxidative damage of cellular macromolecules by in situ generation of ROS.