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Methylmercury inhibits prolactin release in a cell line of pituitary origin.

Maués LA, Macchi BM, Crespo-López ME, Nasciutti LE, Picanço-Diniz DL, Antunes-Rodrigues J, Nascimento JL - Braz. J. Med. Biol. Res. (2015)

Bottom Line: 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.Interestingly, inhibition of nitric oxide synthase by N-nitro-L-arginine completely prevented the decrease in prolactin release without acute neurotoxic effects of methylmercury.

View Article: PubMed Central - PubMed

Affiliation: Laboratório de Neuroquímica Molecular e Celular, Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, PA, Brasil.

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.

No MeSH data available.


Related in: MedlinePlus

Prolactin release (top panel) and cellular viability(bottom panel) of the rat pituitary cell line GH3B6 exposedto different methylmercury (MeHg) concentrations and/or 3 mM N-nitro-L-arginine(L-NARG) for 2 h. Data are reported as means ± SE (n=6). *P<0.05,**P<0.01, and ***P<0.001 vs control and groups incubatedwith L-NARG and L-NARG + MeHg (1 and 10 μM); #P<0.05 and###P<0.001 vs all groups except thoseincubated with 100 μM MeHg and L-NARG + 100 μM MeHg (ANOVA with Tukey'stest).
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f02: Prolactin release (top panel) and cellular viability(bottom panel) of the rat pituitary cell line GH3B6 exposedto different methylmercury (MeHg) concentrations and/or 3 mM N-nitro-L-arginine(L-NARG) for 2 h. Data are reported as means ± SE (n=6). *P<0.05,**P<0.01, and ***P<0.001 vs control and groups incubatedwith L-NARG and L-NARG + MeHg (1 and 10 μM); #P<0.05 and###P<0.001 vs all groups except thoseincubated with 100 μM MeHg and L-NARG + 100 μM MeHg (ANOVA with Tukey'stest).

Mentions: There were no differences in cellular viability and prolactin release, compared withthe control groups, when GH3B6 cells were incubated with 3 mM L-NARG (Figures 2 and 3). Co-incubation of MeHg and L-NARG completely prevented the decrease ofprolactin release seen with 1 and 10 μM MeHg (Figures2 and 3, top panels). However, L-NARGdid not show any protective effect against the decreased release of prolactin whencells were exposed to 100 μM MeHg for 2 h (perhaps because of the significantreduction in cellular viability in those treatment groups). There was no significantdifference in cellular viability between the other groups (Figures 2 and 3, bottompanels).


Methylmercury inhibits prolactin release in a cell line of pituitary origin.

Maués LA, Macchi BM, Crespo-López ME, Nasciutti LE, Picanço-Diniz DL, Antunes-Rodrigues J, Nascimento JL - Braz. J. Med. Biol. Res. (2015)

Prolactin release (top panel) and cellular viability(bottom panel) of the rat pituitary cell line GH3B6 exposedto different methylmercury (MeHg) concentrations and/or 3 mM N-nitro-L-arginine(L-NARG) for 2 h. Data are reported as means ± SE (n=6). *P<0.05,**P<0.01, and ***P<0.001 vs control and groups incubatedwith L-NARG and L-NARG + MeHg (1 and 10 μM); #P<0.05 and###P<0.001 vs all groups except thoseincubated with 100 μM MeHg and L-NARG + 100 μM MeHg (ANOVA with Tukey'stest).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4541687&req=5

f02: Prolactin release (top panel) and cellular viability(bottom panel) of the rat pituitary cell line GH3B6 exposedto different methylmercury (MeHg) concentrations and/or 3 mM N-nitro-L-arginine(L-NARG) for 2 h. Data are reported as means ± SE (n=6). *P<0.05,**P<0.01, and ***P<0.001 vs control and groups incubatedwith L-NARG and L-NARG + MeHg (1 and 10 μM); #P<0.05 and###P<0.001 vs all groups except thoseincubated with 100 μM MeHg and L-NARG + 100 μM MeHg (ANOVA with Tukey'stest).
Mentions: There were no differences in cellular viability and prolactin release, compared withthe control groups, when GH3B6 cells were incubated with 3 mM L-NARG (Figures 2 and 3). Co-incubation of MeHg and L-NARG completely prevented the decrease ofprolactin release seen with 1 and 10 μM MeHg (Figures2 and 3, top panels). However, L-NARGdid not show any protective effect against the decreased release of prolactin whencells were exposed to 100 μM MeHg for 2 h (perhaps because of the significantreduction in cellular viability in those treatment groups). There was no significantdifference in cellular viability between the other groups (Figures 2 and 3, bottompanels).

Bottom Line: 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.Interestingly, inhibition of nitric oxide synthase by N-nitro-L-arginine completely prevented the decrease in prolactin release without acute neurotoxic effects of methylmercury.

View Article: PubMed Central - PubMed

Affiliation: Laboratório de Neuroquímica Molecular e Celular, Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, PA, Brasil.

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.

No MeSH data available.


Related in: MedlinePlus