Acute cobalt exposure and oxygen radical scavengers in the rat myocardium

Biochim Biophys Acta. 1993 Jun 19;1181(3):257-60. doi: 10.1016/0925-4439(93)90029-z.

Abstract

Excessive amounts of cobalt are cardiotoxic, although the mechanism for this toxicity remains unclear. We studied the effects of acute cobalt exposure on the activities of free radical scavengers in the myocardium in 5 groups of rats. Six rats served as a control group and were given a daily subcutaneous injection of 1 ml saline for 8 days. The other 4 groups of rats received a daily injection subcutaneously of cobalt chloride in doses of 1 mg/kg bw, 5 mg/kg bw, 20 mg/kg bw and 50 mg/kg bw, respectively for 8 days. There was a marked and dose-dependent accumulation of cobalt in the myocardium of the cobalt exposed rats. Creatine kinase, copper-zinc superoxide dismutase (CuZn-SOD) and alpha-tocopherol content did not differ between the control and the cobalt exposed groups. The activity of glutathione peroxidase increased, while the activity of manganese-superoxide dismutase (Mn-SOD) was significantly reduced in the cobalt exposed groups. There was an inverse relationship (r = 0.60, P < 0.0001) between the cobalt content and Mn-SOD activity in the myocardium. These results suggest that acute cobalt cardiotoxicity may involve a reduction of intrinsic scavengers resulting in an increased vulnerability to oxygen free radical toxicity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cobalt / toxicity*
  • Dose-Response Relationship, Drug
  • Free Radical Scavengers*
  • Glutathione Peroxidase / metabolism
  • Heart / drug effects*
  • Male
  • Myocardium / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Superoxide Dismutase / metabolism
  • Superoxides / metabolism*
  • Vitamin E / metabolism

Substances

  • Free Radical Scavengers
  • Superoxides
  • Vitamin E
  • Cobalt
  • Glutathione Peroxidase
  • Superoxide Dismutase