Volume 16, Issue 2 pp. 122-126
Research Article

LDH profiles of male and female rats treated with Vepacide

M. F. Rahman

Corresponding Author

M. F. Rahman

Biochemical Toxicology, Biology Division, Indian Institute of Chemical Technology, Hyderabad 500 007, India

Biochemical Toxicology, Biology Division, Indian Institute of Chemical Technology, Hyderabad - 500 007, IndiaSearch for more papers by this author
M. K. J. Siddiqui

M. K. J. Siddiqui

Analytical Toxicology Division, Industrial Toxicological Research Center, Mahatma Gandhi Marg, Post Box No. 80, Lucknow 226 001, India

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Kaiser Jamil

Kaiser Jamil

Biochemical Toxicology, Biology Division, Indian Institute of Chemical Technology, Hyderabad 500 007, India

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First published: 26 March 2002
Citations: 1

Abstract

In the present study we investigated the effect of vepacide, a neem-based compound, on the biochemical target enzyme lactate dehydrogenase (LDH) in different tissues of male and female albino Wistar rats treated orally with 80, 160 and 320 mg/kg (low, medium and high doses, respectively) for a period of 90 days. Prolonged administration of vepacide caused a significant increase of LDH activity in serum and lung tissues and a decrease in liver and kidney in both male and female rats when measured after 45 and 90 days of daily treatment. Females were more susceptible than males with regard to serum and kidney LDH showing sexual dimorphism in the treated rats. Recovery was observed in the affected enzyme after 28 days post treatment (withdrawal study). A positive correlation was observed with regard to this enzyme between serum and lung tissues, whereas for serum versus liver and kidney there was a negative correlation. The effect of vepacide was more pronounced in the lung tissue followed by liver and kidney tissues. Necrosis of the liver and kidney tissues was observed but in the lung tissue an increase in the LDH enzyme was seen. Therefore, it was concluded that the increase in LDH could be indicative of a stress adaptive response to the toxicant. Copyright © 2002 John Wiley & Sons, Ltd.

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