Methylmercury inhibits prolactin release in a cell line of pituitary origin

• Main Authors: L.A.L. Maués, B.M. Macchi, M.E. Crespo-López, L.E. Nasciutti, D.L.W. Picanço-Diniz, J. Antunes-Rodrigues, J.L.M. do Nascimento
• Format: Article
• Language: English
• Published: Associação Brasileira de Divulgação Científica 2015-08-01
• Series: Brazilian Journal of Medical and Biological Research
• Subjects: Mercury; Methylmercury; Prolactin; Oxidative stress; Pituitary; Nitric oxide
• Online Access: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2015000800691&lng=en&tlng=en

Heavy metals, such as methylmercury, are key environmental pollutants that easily reach human beings by bioaccumulation through the food chain. Several reports have demonstrated that endocrine organs, and especially the pituitary gland, are potential targets for mercury accumulation; however, the effects on the regulation of hormonal release are unclear. It has been suggested that serum prolactin could represent a biomarker of heavy metal exposure. The aim of this study was to evaluate the effect of methylmercury on prolactin release and the role of the nitrergic system using prolactin secretory cells (the mammosomatotroph cell line, GH3B6). Exposure to methylmercury (0-100 μM) was cytotoxic in a time- and concentration-dependent manner, with an LC50 higher than described for cells of neuronal origin, suggesting GH3B6 cells have a relative resistance. Methylmercury (at exposures as low as 1 μM for 2 h) also decreased prolactin release. Interestingly, inhibition of nitric oxide synthase by N-nitro-L-arginine completely prevented the decrease in prolactin release without acute neurotoxic effects of methylmercury. These data indicate that the decrease in prolactin production occurs via activation of the nitrergic system and is an early effect of methylmercury in cells of pituitary origin.