Abstract
Intoxication with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produced marked increases in cellular smooth endoplasmic reticulum content and microsomal drug metabolizing enzyme activity in kidney cortex. Therefore, it was of interest to determine the effect of TCDD on several proximal tubular functions. Adult rats were treated with 10, 25, and 50 μg/kg, TCDD. Ten μg/kg TCDD 3 or 7 days after treatment did not affect p-aminohippurate (PAH) accumulation by renal cortical slices. N-methylnicotinamide (NMN) accumulation was slightly decreased following this treatment. At 25 μg/kg, TCDD decreased the capacity of renal tissues to transport both PAH and NMN 7 days after exposure. The increase in ammoniagenesis and gluconeogenesis observed in acidosis was not significantly different in animals that had been treated with 25 μg/kg TCDD 7 days before experimentation. Glomerular filtration rate and effective renal plasma flow were decreased in rats after 25 or 50 μg/kg TCDD. Volume expansion did not alter this relationship. Fractional sodium excretion was less than 1% in both control and TCDD-treated animals. With volume expansion sodium excretion increased to approximately 5% and was not different for control and TCDD-treated animals. TCDD enhanced several hepatic and renal drug metabolizing enzyme systems but did not alter the acute toxicity of CHC13.
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© 1978 Plenum Press, New York
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Hook, J.B., McCormack, K.M., Kluwe, W.M. (1978). Renal Effects of 2,3,7,8-Tetrachlorodibenzo-p-dioxin. In: Rao, K.R. (eds) Pentachlorophenol. Environmental Science Research, vol 12. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-8948-8_33
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DOI: https://doi.org/10.1007/978-1-4615-8948-8_33
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