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Carcinogenesis Advance Access published online on August 29, 2003
Carcinogenesis, doi:10.1093/carcin/bgg161
© 2003 by Oxford University Press
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© 2003 Oxford University Press

CARCINOGENESIS

Diallyl sulfide inhibits the oxidation and reductions reactions of stilbene estrogens catalyzed by microsomes, mitochondria, and nuclei isolated from breast tissue of female ACI rats

Ronald D. Thomas 1*, Mario R. Green 1, Chantell Wilson 1, and Sakeenah Sadrud-Din 2

1 Environmental Toxicology Program, College of Pharmacy and Pharmaceutical Sciences, Florida A&M University, Tallahassee FL 32307
2 Biology Department, College of Arts and Sciences, Florida A&M University, Tallahassee FL 32307

* Corresponding author. E-mail: ronald.thomas{at}famu.edu.

Received 1 May 2003 ; revised 6 August 2003 ; accepted 19 August 2003

Abstract

Previously it has been demonstrated that microsomal, mitochondrial, and nuclear enzymes isolated from the liver of male Sprague Dawley rats catalyzed the oxidation of diethylstilbestrol (DES) to DES quinone. In the present study we have shown that diallyl sulfide (DAS) inhibits the oxidation of DES to DES quinone in all three sub cellular fractions (microsomes, mitochondria, and nuclei) isolated from breast tissue of female ACI rats. UV analysis of mitochondrial and microsomal fractions revealed that DAS decreased the rate of DES oxidation to DES quinone and DAS also decreased the rate in which DES quinone was reduced to DES. Lineweaver-Burk plots of the rate of DES quinone formation at various DES and DAS concentrations demonstrated that DAS inhibited the oxidation of DES and the reduction of DES quinone in a noncompetitive fashion. In both microsomal and mitochondrial oxidation reactions the Km remained constant whereas the Vmax decreased with increasing DAS (0, 186, & 373 µM) concentrations (microsomes Km = 80 µM; Vmax = 5.56, 4.16 & 3.33 nmole/mg protein/min; mitochondria Km= 35.7 µM; Vmax = 3.45, 2.44 & 1.82 nmole/mg protein/min). Results were similar for reduction reactions. HPLC analysis revealed that a concentration of 186 µM DAS inhibited the mitochondrial, microsomal, and nuclear oxidation by 27%, 35%, and 40% respectively. A concentration of 373 µM DAS inhibited the mitochondrial, microsomal, and nuclear oxidation by 50%, 52%, and 60% respectively. These data provide direct evidence that the breast tissue contain the metabolic machinery required to oxidize DES to reactive intermediates that may lead to genetic instability and cancer. This inhibition may play a role in the chemoprevention of stilbene estrogen-induced breast cancer.


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