Mechanism of Testicular Interstitial Cell Damage by Heavy Metal Lead Based on Computer-aided Technology

Abstract

Objective: To explore the toxicological effect of heavy metal lead on testicular interstitial cells by detecting the gene expression levels of enzymes related to injury healing, to provide an experimental basis for revealing the toxicological mechanism of heavy metal-induced male sexual dysfunction. Methods: The r2c cell line of testicular interstitial cell was exposed to a serum-free culture environment containing heavy metal lead. The activity of the cells was determined at 1, 3, 6, 12, and 24 h. The supernatant of the cells was collected to detec the changes in the injury healing by computer-aided technology. The RT-RCR method was used to observe the differences in the gene expressions of injury healing related enzymes. Results: CCK-8 assay showed that the vicapacity of r2c cells was not significantly reduced after they were exposed to 100 μmol/L heavy metal lead for 12 and 24 h (P > 0.05). Computer-aided radioimmunoassay was used to detect the changes in the progesterone, and the results showed that the synthesis of progesterone was significantly reduced at 12 and 24 h (P < 0.05). After the cells were exposed to the medium containing lead, the expressions of the steroid hormone synthetase gene returned to the normal level after 12 and 24 h. However, the expressions of StAR and P450scc genes decreased significantly after exposure to lead for 3 h (P < 0.05), and the expressions of the StAR gene decreased even more dramatically after exposure to lead for 6 h (P < 0.01). Conclusions: Heavy metal lead can inhibit the synthesis of progesterone in r2c cells mainly by down-regulating the gene expression levels of cholesterol transporter StAR and rate-limiting enzyme P450scc in the injury healing pathway.