In utero and lactational exposure of carbofuran to rats: effect on testes and sperm

Hum Exp Toxicol. 1997 May;16(5):267-72. doi: 10.1177/096032719701600506.

Abstract

Male offspring of adult females treated with 0.2 or 0.4 mg/kg during either the whole of pregnancy or the whole of the lactation period did not induce generalised toxic effects. A significant alteration in enzymatic activities i.e. SDH (decreased), LDH and Y-GT (increased) were observed in testes only at 0.4 mg/kg. A decrease in sperm motility, sperm count along with increase in percent abnormal sperm was observed at 0.4 mg/kg dose level. Histopathological examination revealed loss of spermato-genesis, degenerative changes in Sertoli cells which are well supported with biochemical studies indicating that carbofuran interferes with the maturation process of testis. No such effects were observed at 0.2 mg/kg. The testicular and spermatotoxic effects observed in rats given in utero or lactational exposure may be due to transfer of carbofuran or its metabolites through placenta or mothers milk.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Suckling
  • Carbofuran / toxicity*
  • Cholinesterase Inhibitors / toxicity*
  • Female
  • Insecticides / toxicity*
  • L-Iditol 2-Dehydrogenase / metabolism
  • L-Lactate Dehydrogenase / metabolism
  • Lactation
  • Male
  • Pregnancy
  • Prenatal Exposure Delayed Effects*
  • Rats
  • Sperm Motility / drug effects
  • Spermatozoa / cytology
  • Spermatozoa / drug effects*
  • Spermatozoa / physiology
  • Testis / drug effects*
  • Testis / enzymology
  • Testis / pathology
  • gamma-Glutamyltransferase / metabolism

Substances

  • Cholinesterase Inhibitors
  • Insecticides
  • L-Iditol 2-Dehydrogenase
  • L-Lactate Dehydrogenase
  • gamma-Glutamyltransferase
  • Carbofuran