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Journal of Environmental Pathology, Toxicology and Oncology
Fator do impacto: 1.241 FI de cinco anos: 1.349 SJR: 0.356 SNIP: 0.613 CiteScore™: 1.61

ISSN Imprimir: 0731-8898
ISSN On-line: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.2013006505
pages 73-90

Pre- and Postnatal Toxicity of Diazinon Induces Disruption of Spermatogenetic Cell Line Evidenced by Increased Testicular Marker Enzymes Activities in Rat Offspring

Srinivasa Jayachandra
School of Medicine, Universiti Malaysia Sabah, 88400 Kota Kinabalu Sabah, Malaysia
Urban JA D'Souza
School of Medicine, Universiti Malaysia Sabah, 88400 Kota Kinabalu Sabah, Malaysia

RESUMO

The objective of this study was to study the possible reproductive adverse effects of the diazinon on rat offspring exposed in utero and during lactation. Dams were gavaged daily (10, 15, and 30 mg/kg) before mating, during mating, and during pregnancy and lactation in separate groups. Reproductive outcome data of dams were examined. Body weight, testis weight, testicular marker enzyme activities (alkaline phosphatase, acid phosphatase, lactate dehydrogenase, and glucose-6-phosphate dehydrogenase), qualitative and quantitative testicular and epididymal histology, and immunohistochemisty for 3-β-hydroxysteroid dehydrogenase (HSD) were examined in male offspring at puberty and adulthood. The 30-mg/kg dose induced significant adverse effects at both puberty and adulthood in offspring. At puberty the male offspring showed a decrease in testicular weight, degenerative changes, and 3-β-HSD. Moreover, an increase in activity of alkaline and acid phosphatase also was observed. At adulthood, there was a decrease in testicular weight and 3-β-HSD with an increase in the levels of testicular marker enzyme. There was evidence of some adverse reproductive effects in male offspring at the 15-mg/kg dose. Most of the adverse effects were irreversible and were evident at both puberty and adulthood in offspring, although a few parameters reverted back to the normal growth pattern. Hence, diazinon is a reproductive toxicant in male offspring, which caused significant damage to the testes when exposed during prenatal and postnatal life.

Palavras-chave: diazinon, off springs, 3-β, -HSD, LDH

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