Effects of methiocarb on lipid peroxidation and glutathione level in rat tissues


Ozden S., Alpertunga B.

DRUG AND CHEMICAL TOXICOLOGY, cilt.33, sa.1, ss.50-54, 2010 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 33 Sayı: 1
  • Basım Tarihi: 2010
  • Doi Numarası: 10.3109/01480540903130708
  • Dergi Adı: DRUG AND CHEMICAL TOXICOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.50-54
  • Anahtar Kelimeler: Methiocarb, lipid peroxidation, glutathione, liver, kidney, brain, testis, N-METHYLCARBAMATE PESTICIDES, INDUCED OXIDATIVE STRESS, REDOX SYSTEM, CARBAMATE, ENZYMES, WATER, MALONDIALDEHYDE, ANTIOXIDANTS, SULFOXIDE, RESIDUES
  • İstanbul Üniversitesi Adresli: Evet

Özet

Methiocarb is an N-methylcarbamate insecticide used worldwide in agriculture and health programs. The aim of this study was to investigate the possible effects of methiocarb to induce lipid peroxidation (LPO) in tissues of male Wistar rats following single and repeated oral exposures. Animals were divided into six different groups, and methiocarb was administered by orally at doses 25, 10, and 2 mg/kg body weight for 1, 5, and 28 days, respectively. Liver, kidney, brain, and testis tissues were taken from the rats for the biochemical examinations. LPO and reduced glutathione (GSH) levels were determined in the tissues. LPO was significantly increased in liver, kidney, brain, and testis after 1-, 5-, and 28-day treatments of methiocarb. GSH levels were significantly increased in the I-day period and significantly decreased in the 5- and 28-day periods in all tissues after methiocarb administration. It is concluded that methiocarb may induce LPO and produce disturbances on the GSH levels in liver, kidney, testis, and brain of rats. This suggests that methiocarb-induced toxicity may be associated with oxidative stress to cellular membranes. Further studies are required to better understand the role of oxidative stress on methiocarb-induced toxicity.