Abstract
Intoxication with 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD) results in 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, intraperitoneally, or 1 and 5 μg, intragastrically, TCDD. Neither intragastric dose of TCDD had a significant effect on the ability of renal cortical slices to accumulate p‐aminohippuric acid (PAH) 7 days after treatment. Similarly, 10 μg/kg TCDD 3 or 7 days after treatment did not affect PAH accumulation. 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. Accumulation of 2‐deoxyglucose was unaffected by TCDD. The increase in ammoniagenesis and gluconeo‐genesis observed in acidotic states was not significantl...
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