ABSTRACT
OBJECTIVE: To study the effect of myricetin and its mechanism for spermatogenesis obstruction caused by lead acetate in male mice. METHODS: The spermatogenesis obstruction of male mice model was built by intraperitoneal injection with lead acetate(20 mgkg-1) for 7 d. From the 2 d model made mice in low, medium and high doses myricetin were treated by myricetin, respectively(100, 200, 400 mgkg-1) by intraperitoneal injection for 42 d. The mice were sacrificed on day 43 for the measurement of the sperm density and sperm aberration rate. The levels of lactate dehydrogenase(LDH), nitric oxide(NO), tumor necrosis factor α(TNF-α) in testicular tissue homogenate, the content of malondialdehyde(MDA) in blood serum were assayed respectively. The pathological changes of testicular tissues were observed. RESULTS: Compared with the model group, sperm density was increased, the sperm aberration rate mice were decreased, the activities of LDH in testicular tissue homogenate were improved and the contents of NO in testicular tissue homogenate were decreased in different doses myricetin groups. The activities of TNF-α in testicular tissue homogenate and the content of MDA in blood serum were increased. Pathological change of testis showed there were decline of spermatogenic cells in levels and numbers and few spermiogenesis in most of seminiferous tubule in model group. Those change above could be reversed by myricetin. CONCLUSION: Myricetin has certain improvement on spermatogenesis obstruction of mice caused by lead acetateits, its mechanism may be related to decreasing NO, anti-oxidation and inhibiting inflammatory mediator.