Effects of vanadium(V) and/or chromium(III) on L-ascorbic acid and glutathione as well as iron, zinc, and copper levels in rat liver and kidney.

This study investigated the selected parameters of the antioxidant system in liver and kidney after in vivo administration of vanadium and/or chromium in rats. Outbred 2-mo-old albino male Wistar rats received drinking water for 12 wk with either sodium metavanadate (SMV; group II); chromium chloride (Cr; group III); or sodium metavanadate and chromium chloride (SMV-Cr; group IV); and group I (control) received deionized water. Chronic treatment with V alone or in combination with Cr produced a significant increase in kidney relative weight. Further, giving rats V alone also led to a significant elevation in liver relative weight. An increase in hepatic Fe concentration and renal Zn content occurred after treatment with V or Cr, respectively. The rats coadministered V and Cr had significantly higher levels of Fe in liver and Zn in kidneys. Simultaneous administration of these two elements resulted in a significant decrease in renal L-ascorbic acid concentration. V given alone significantly decreased GSH content and GSH/GSSG ratio in liver and kidney as well as increased GSSG concentration in liver, whereas Cr alone produced a significant decrease in GSH content in kidney and GSH/GSSG ratio in both organs. In the SMV-Cr-treated group a significant decrease in renal GSH concentration and GSH/GSSG ratio in both organs occurred. A significant increase in liver GSSG content was also found. The observed significant changes in kidney GSH content and in GSH/GSSG ratio in both rat tissues after Cr might result from the pro-oxidant actions of this metal. Thus, oxidative stress, which is a major pathway for V-induced toxicity, might also be associated with Cr(III)-induced adverse effects in rats.