Methylmercury inhibits prolactin release in a cell line of pituitary origin

Abstract

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.

Towards Therapeutic Alternatives for Mercury Neurotoxicity in the Amazon: Unraveling the Pre-Clinical Effects of the Superfruit Açaí (Euterpe oleracea, Mart.) as Juice for Human Consumption

“…Lipid peroxidation responsible for MeHg-induced neurotoxicity may also be associated with increased nitrite levels (as an indirect marker of nitric oxide production) [18,59,60]. It has already been demonstrated that some of the initial effects of MeHg on cells of CNS origin occur via activation of the nitrergic system [60,61,62]. Here, we found increased nitrite levels in the brains of the exposed animals (Figure 6), confirming this activation of the nitrergic system as a relevant effect of MeHg-induced neurotoxicity (when no major change was detected in spontaneous neurological behavior).…”

Diphenyl diselenide protects against methylmercury‐induced inhibition of thioredoxin reductase and glutathione peroxidase in human neuroblastoma cells: a comparison with ebselen

“…In fact, the study of more than one type of cells can give more details about the molecular mechanisms involved in the neurotoxicity of MeHg. However, several studies, as evidenced in the present investigation, have been successfully performed using a single cell line, either from neuronal and non‐neuronal origin, to determine the biochemical mechanism(s) underlying MeHg toxicity (Branco et al ., ; Carvalho et al ., ; Crespo‐Lopez et al ., ; Fujimura and Usuki, ; Maués et al ., ; Sakaue et al ., ; Zimmermann et al, ).…”

Poisonings with heavy metals and neoplasms - possible correlations

“…This dual effect can be explained by different interactions between the types of mercury (inorganic and organic) and the secretion of PRL by the pituitary gland, which is controlled by neural-transmitters, such as dopamine. Thus, it has been suggested that serum PRL can be a possible biomarker of exposure to heavy metals (Maues et al, 2015).…”