Cadmium induced-oxidative stress in pituitary gland is reversed by removing the contamination source.
Cadmium (Cd(2+)) is one of the most important environmental contaminants and acts as an endocrine disruptor. Previously, we have demonstrated that the simultaneous administration of Cd(2+) and melatonin (Mel) in drinking water impaired metal-induced oxidative stress in rat anterior pituitary gland. The aim of this study was to investigate if a treatment started after the toxic manifestations of Cd( 2+) became evident could reverse the effects of the metal. Animals exposed to Cd(2+) (5 parts per million [ppm], 30 days) were treated with Mel or without the metal during the next 1 or 2 months. Cd(2+) exposure increased the expression of heme oxygenase-1 (HO-1), a biomarker of oxidative stress, and an a posteriori Mel treatment reversed oxidative stress induced by Cd(2+). This effect was also observed 1 month after metal removal. The Cd(2+)-induced increase in metallothionein-1 (MT-1) and nitric oxide synthase 1 (NOS1) expression were also reversed by metal removal. In addition, serum prolactin and luteinizing hormone levels affected by Cd( 2+) exposure were normalized. Considering that the manifestations of Cd(2+) intoxication become evident only after a certain period of metal accumulation, these results show that metal removal is enough to reverse Cd(2+) effects in anterior pituitary gland and bring to light the relevance of moving away the individual from the contamination source.
Miler
Eliana A
EA
Departamento de Química Biológica, IQUIFIB, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.
Nudler
Silvana I
SI
Quinteros
Fernanda A
FA
Cabilla
Jimena P
JP
Ronchetti
Sonia A
SA
Duvilanski
Beatriz H
BH
D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D019256:Cadmium Chloride / Q000633:toxicity*; D004785:Environmental Pollutants / Q000633:toxicity*; D015870:Gene Expression / Q000187:drug effects; D006419:Heme Oxygenase (Decyclizing) / Q000235:genetics / Q000378:metabolism; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D008550:Melatonin / Q000494:pharmacology*; D008668:Metallothionein / Q000235:genetics / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000235:genetics / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I; D018384:Oxidative Stress / Q000187:drug effects*; D010903:Pituitary Gland, Anterior / Q000187:drug effects*; D011388:Prolactin / Q000097:blood; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D020127:Recovery of Function / Q000187:drug effects*
D015415:Biomarkers; D004785:Environmental Pollutants; C491055:Mt2A protein, rat; D012333:RNA, Messenger; D011388:Prolactin; D007986:Luteinizing Hormone; D008668:Metallothionein; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; C496322:Nos1 protein, rat; D006419:Heme Oxygenase (Decyclizing); C491523:Hmox1 protein, rat; D019256:Cadmium Chloride; D008550:Melatonin