Abstract
Arsenic is a
broad-spectrum environmental contaminant with mutagenic, teratogenic and
carcinogenic effects. Due to its widespread distribution in nature, drinking
water is the most common source of arsenic exposure for the general population.
In this study, we aimed to determine the effect of sodium arsenite on the
viability and expression profile of steroidogenic genes in TM3 Leydig cells,
responsible for testicular steroidogenesis. The TM3 Leydig cells were treated
with sodium arsenic (384,8 µM or 7,6 mM) for 24 hours with LH (Luteinizing
hormone) stimulation. The MTT assay was used for measuring cell viability, the
expression level of key genes of the steroidogenesis was evaluated using
RT-qPCR.The MTT assay showed that cell viability was decreased dose-dependently.
RT-qPCR demonstrated that the expression level of CYP11A1, CYP17A1 were
decreased as compared to the untreated control while StAR gene expression was
found to be surprisingly high in the cell exposed to high-dose arsenic (p<0.05). The expression profile of
two dehydrogenase; 17β-HSD and 3β-HSD was significantly reduced in high dose
arsenic treated-group (p<0.05);
but however, no statistical significance was found in low-dose. The RT-qPCR
also showed that the expression SF-1 (Steroidogenic factor-1), a key regulator
of adrenal and reproductive development, was significantly decreased in both
low-dose and high-dose (p<0.05).
Arsenic toxicity in Leydig cell leads to cell viability loss and cause a
perturbation in key steroidogenic genes, reflecting the possible role of
arsenic in infertility and male reproductive system disorders.