The Study Of Lead Exposure On Male Reproductive Toxicity In Mice

The deterioration of male fertility, found in numerous epidemiological studies of past decades,can be connected to growing exposure to environmental toxins. Heavy metals, especially lead is widely spread and extremely toxic. The mechanism by which lead exerts toxic effects on testis is quite complex. It involves spermatogenesis, steroidogenesis, and red-ox system. The chronic lead exposure can induce functional disorder (decrease of testosterone synthesis) or morphological disorder (decrease of testicular weight and seminal vesicle, peritubular fibrosis, seminiferous tubular diameter decrease and decrease in germ cell population related to an apoptotic process). Currently existing environmental and occupational exposure to lead and increasing combined exposure to environmental toxins results in constantly increasing number of diagnosed fertility impairments.To study the influences of the lead on male reproductive function.This study builds three experimental groups(1/10LD50,1/50LD50,1/250LD50) and control group in intraperitoneal injection.we use some technical means including blood cell count plate, single-cell gel electrophoresis, terminal deoxynucleotidyl transferase tag (TUNEL) to study semen quality, testicular morphology, testicular tissue protein, redox level and relative enzyme activities, DNA damage, testis cell apoptosis caused by lead. The results showed:1. High dose group of the mice's body weight increasing was significantly lower than the control group after 30d.And the survival ratio of sperm significantly reduced in lead poisoning after 40d.The sperm abnormality rate of experimental group was significantly increased.Lead poisoning after long-term,the sperm effect of damage and reduction was obvious.2. Compared with the control group,the experimental group's GSH-PX, SOD activity decreased and MDA increased, while the SOD / MDA was significantly lower than the control group.The protein content of the experimental group were significantly decreased.3. After 40 d,50 d,60 d by lead poisoning,which can lead to he mouse testis cells's DNA single-strand breaks.Mean while, the tailed-cells rates and DNA damage unit increased. With the lead exposure time lasting, the DNA damage were more and more serious.Lead exposure after 60 d.,the high dose group's tailed-cells rates reach 89.8% and DNA damage reach 184.2.4. After lead exposure,The mouse testis's spermatogenic cells, seminiferous tubules and interstitial cells were obviously pathological changes, and the high dose group testicular tissue damage even worse. HE staining shows the seminiferous small tube cavity has loss of spermatogenic cells. Meanwhile, TUNEL assay showed that mouse spermatogenic cells at all levels exist in apoptosis. High dose group testicular cells apoptosis rate was significantly and pathologically increased.In conclusion, lead acetate exposure resulted from macroscopic feather(tissues and organs)to molecular level(cell and DNA) damaged, and making reproductive function significantly decreased. The mechanisms of its toxicity is likely to lead directly to damage of spermatogenic epithelium, resulting in degenerative changes in testes and sperm damage reduction, energy reduction and deformity.Meanwhile it induced oxidative stress in testicular tissue and inhibiting the activity of antioxidant enzymes.The result was increasing testicular DNA strand breaks and accelerating the apoptosis process.