Graduate Thesis Or Dissertation
 

The effects of 1, 1, 1-Trichloro-2, 2-bis (p-chlorophenyl)ethane on the in vivo metabolism of acetate in rats

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  • A single oral dose of DDT, ranging from 40 to 200 mg/kg, had a drastic effect on the in vivo acetate metabolism in rats. The normal elimination pattern of the expired ¹⁴CO₂ from ¹⁴C-labelled acetate was distorted, and the rate of output of the ¹⁴CO₂ was decreased. The ratio of two labelled urinary metabolites, urea and one unknown compound, was also affected by DDT. Both of these were dependent upon the dosage level and the time of post-adminis tration. DDT affected differently the C-1 and C-2 carbons of acetate molecule on the ¹⁴CO₂ elimination patterns and the incorporation into urinary metabolites, suggesting that these two carbons went through different pathways of metabolism. No such effect was observed when labelled acetate was given intraperitoneally, suggesting that the absorption mechanism of the gastro-intestinal tract may be involved. DDT slowed down the in vitro active transport of acetate-1-¹⁴C across the rat intestine. Within two hours, as much as 57 percent inhibition was observed in the transport of acetate-1-¹⁴C from the mucosal to the serosal side of DDT-treated intestine at 25°C. DDT increased the incorporation of acetate-1-¹⁴C into total liver lipids, this increase being due to the increased incorporation of ¹⁴C into the neutral lipids and the decreased incorporation into phospholipids. No significant difference was found in the liver neutral lipids of the DDT-treated and control rats, but an alternation in the distribution of ¹⁴C-labelled phospholipid was observed in the DDT-treated rats. This change in the abundance of ¹⁴C-labelled phospholipids in rat liver was concluded to be due to the inhibition of transmethylation and decarboxylation by DDT.
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