Effect of sulfite exposure on zinc, iron, and copper levels in rat liver and kidney tissues


Kucukatay V., Turgut S., Kocamaz E., Emmungil G., Bor-Kucukatay M., Turgut G., ...Daha Fazla

Biological Trace Element Research, cilt.114, sa.1-3, ss.185-195, 2006 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 114 Sayı: 1-3
  • Basım Tarihi: 2006
  • Doi Numarası: 10.1385/bter:114:1:185
  • Dergi Adı: Biological Trace Element Research
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.185-195
  • Anahtar Kelimeler: Copper, Iron, Kidney, Liver, Sulfite, Sulfite oxidase, Zinc
  • Ondokuz Mayıs Üniversitesi Adresli: Hayır

Özet

Sulfite is a potentially toxic molecule that might enter the body via ingestion, inhalation, or injection. For cellular detoxification, mammalians rely on sulfite oxidase to convert sulfite to sulfate. The purpose of this research was to determine the effect of sulfite on zinc, iron, and copper levels in rat liver and kidney tissues. Forty normal and sulfite oxidase-deficient male albino rats were divided into four groups that included untreated controls (group C), a sulfite-supplemented group that received 70 mg sodium metabisulfite per kilogram per day (group S), a sulfite oxidase- deficient group (group D), and a sulfite oxidase-deficient group that was also given 70 mg sodium metabisulfite per kilogram per day (group DS). The iron and zinc levels in the liver and kidney in groups S and DS were not affected by sulfite treatment compared to their respective controls (groups C and D). Sulfite exposure led to an increase of kidney copper content in the S group when compared to untreated controls. The kidney copper levels were significantly increased in the unexposed deficient rats, but it was not different than that of the deficient rats that were given oral sulfite treatment. These results suggest that kidney copper levels might be affected by exogenous or endogenous sulfite. © Copyright 2006 by Humana Press Inc.