Authors: KONAN Kouassi Martin, ADON Arsene, N’GUESSAN Assue Julien, SYLLA, Aboubakar, OBRO Koby Albert, N’GUESSAN Jean David, DJAMAN allico Joseph, DOSSO Mireille
Epidemiological studies of male workers with blood lead levels have shown that they increase the risk of infertility. Several studies on the reproductive system of male animals have also shown that lead is toxic to testicular function. However, the mode of action of lead on male reproductive functions remains poorly studied. The aim of this study was therefore to elucidate the mechanism by which lead induces male infertility. Ten male Wistar rats were divided into an experimental group (N=5) and a control group (N=5). The control group received sterile distilled water while the experimental group received a 0.3% lead acetate solution for 90 consecutive days. At the end of the experiment, the rats were euthanised. Blood was collected from the rats by cardiac puncture for the determination of malondialdehyde (MDA). The left testis was isolated for assessment of apoptosis using the Tunel method. Part of the right testis was used to assess the expression of apoptotic and oxidative genes by RT-PCR and the other part for the production of testicular homogenates. The results showed a highly significant increase in the concentration of MDA in the blood and testicular homogenates of rats from the experimental batch compared with rats from the control batch. The results also showed a highly significant increase in the number of apoptotic cells (p=0.0002) in rats from the experimental batch. This study highlights the mechanism by which lead induces male infertility. It shows that exposure to lead causes oxidative stress correlated with excessive cell proliferation due to underexpression of P53. This cell proliferation induces more abundant apoptosis of germ cells, which could explain the drop in male fertility.
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