@article {Novelli:1999:0960-3123:109,
title = "Superoxide radical and nephrotoxic effect of cadmium exposure",
journal = "International Journal of Environmental Health Research",
parent_itemid = "infobike://tandf/cije",
publishercode ="tandf",
year = "1999",
volume = "9",
number = "2",
publication date ="1999-06-01T00:00:00",
pages = "109-116",
itemtype = "ARTICLE",
issn = "0960-3123",
eissn = "1369-1619",
url = "https://www.ingentaconnect.com/content/tandf/cije/1999/00000009/00000002/art00003",
doi = "doi:10.1080/09603129973245",
keyword = "SUPEROXIDE RADICAL, ENVIRONMENTAL, CADMIUM, NEPHROTOXICITY",
author = "Novelli, Ethel L.B. and Lopes, Ana M. and Rodrigues, Ana S. and Filho, Jose L.V.B. Novelli and Ribas, Bartolome O.",
abstract = "Pollution and industrial practices result in concentrations of metals and other environmental agents that are related to environmental toxicity. Concentrations of metals are widely related to biochemicals values which are used in disease diagnosis due to environmental toxicity. This work was carried out in order to verify the nephrotoxic effect of cadmium and to clarify the contribution of reactive oxygen species (ROS) in this process. Cadmium chloride was tested for nephrotoxic damage in rats by a single intraperitoneal (i.p.) injection Cd2+ (2 mg/kg) and oral intake (Cd2+ -100mg/l-from CdCl2). The cadmium-induced biochemical alterations included significant increased levels of serum creatinine concentrations, in rats with i.p. injection. Total urinary protein concentrations were only increased in rats with cadmium intake. Lipoperoxide was also increased after 3 and 7 days of the Cd2+ treatment. No changes were observed in glutathione peroxidase activities. Cadmium-induced damage might be due to superoxide radicals (O2-), since Cu-Zn superoxide dismutase activities were decreased by Cd2+ treatment. This study allows tentative conclusions to be drawn regarding which reactive oxygen metabolites play a role in cadmium nephrotoxicity. We concluded that the superoxide radical may be produced as a mediator of nephrotoxic action of cadmium.",
}