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Dietary Selenium and Antioxidant Status: Toxic Effects of 1,2-Dimethylhydrazine in Rats^1,2,

Department of Pathology, Texas Tech University Health Sciences Center, Lubbock, TX 79430

Weanling male Sprague-Dawley rats were used to determine whether the mechanism of the previously reported toxicity of 1,2-dimethylhydrazine (DMH) in selenium-deficient rats was related to a diminished capacity for detoxification of reactive oxygen species via glutathione peroxidase (GSH-Px) as well as by other known pathways of detoxification, including catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GST) and levels of glutathione (GSH). A 3 x 3 factorial experimental design was used to examine the acute effects of DMH treatment (0, 10 and 20 mg/kg body weight) interacting with dietary Se levels (< 0.02, 0.1 and 0.5 mg/kg diet as sodium selenite). Animals were maintained on the test diets for 4 wk prior to challenge with DMH. Preliminary kinetics studies indicated the most appropriate time to examine antioxidant status was 3 h after DMH injection. At that time, livers and colons were analyzed for tissue levels of GSH-Px, CAT, SOD, GST and GSH. Data analysis demonstrated that Se deficiency impaired the ability of both liver and colon to mount an induced detoxification response to the acute oxidative stress generated by DMH challenge and may explain the toxicity of DMH in Se-deficient rats.

KEY WORDS: • selenium • glutathione peroxidase • superoxide dismutase • 1,2-dimethylhydrazine • rats

¹ Presented in part at the 73rd Annual Meeting of the Federation of American Societies for Experimental Biology, New Orleans, LA, March 19–23, 1989 [Pence, B. C. (1989) Reactive oxygen species and selenium deficiency: toxic effects of 1,2-dimethylhydrazine. FASEB J. 3: A779 (abs.)].

² This research was supported by the Institute for Nutritional Sciences of Texas Tech University and Health Sciences Center.

Manuscript received 16 March 1990. Revision accepted 6 June 1990.