Long Term Exposure To Manganese Improves The Expression Of Glutathione
Peroxidase and NADP(H) quinone Oxidoreductase In Adrenal Gland Of Adult
Rats
Posser, T.1; Zemolin, A.P.2; Meinerz, D.F.2; Ternes, A.P.1; Nogueira, A.B. 1 ; da
Silva, G.F.; 1; Rocha, J.B.T2; Franco, J.L2.
1
Campus São Gabriel, Universidade Federal do Pampa, São Gabriel, Rio
Grande do Sul 97300-000, Brazil
2
Departamento de Química, Centro de Ciências Naturais e Exatas,
Universidade Federal de Santa Maria, Santa Maria, RS, 97105-900, Brazil
([email protected])
Adrenal glands (AG) secrete catecholamines which have many functions in the
organism, influencing activities of many tissues. Manganese is an essential
metal, whose long term exposure has been associated with neurological
symptoms similar to observed in Parkinson’s Disease characterizing the
Manganism syndrome. Cathecolaminergic system has been considered an
important target of Manganese toxicity. In this aspect, considering the
importance of AG in the production of catecholamine, our study aims to analyze
the damage caused by long term exposure to Manganese on AG investigating
activity and expression of antioxidant enzymes as well as the expression of
MAPKs, and HSP70 as an indicative of cell response to stress. A possible
damage to catecholaminergic neurons of AG was investigated analyzing
Tyrosine Hidroxilase expression. In this study, Wistar adult rats were treated for
90 days with MnCl2 diluted in drink water at concentration of 120 mg/L.
Subsequently the adrenal medulla was removed for biochemical analysis. The
treatment resulted in an increased activity of Glutathione Pexoxidase with
parallel induction of GPx1 isoform and NADP(H) Quinone Oxidoreductase
(NQO-1) expression. All other proteins investigated in this study were not
altered as well as the content of TH and PARP cleavage, indicating no neuronal
loss. The data reported here show that long term treatment with Manganese
did not induce prominent cell damage in adrenal gland. On the other hand the
increased expression of NQO-1 and GPx1 and increased GPx activity may
represent a biochemical adaptation of AG to prolonged oxidative stress induced
by long term treatment with manganese.
Word Keys: Manganese, adrenal gland, glutathione peroxidase
Supported by: FAPERGS, CNPq and UNIPAMPA