Abstract

Serum β-glucuronidase (β-Glu) activity markedly increased (up to 400-fold) 2, 4, and 6 hours after ip administration of sublethal doses of paraoxon to rats; activity returned to normal 18 hours after treatment. Doses of paraoxon ( 1 8 the LD50) produced no cholinergic signs and had no effect upon erythrocyte, serum, or brain cholinesterase (ChE). However, they increased serum β-Glu 2, 4, and 6 hours after administration; activity returned to control values 18 hours later. Liver β-Glu activity was only slightly increased. Single oral doses ( 1 2 and 1 4 the LD50) of Banol increased serum β-Glu activity when measured 30, 60, and 120 min later. The increases were much lower than the serum β-Glu elevations after paraoxon and were of shorter duration. Neither serum ChE nor liver β-Glu activities were affected. Prolonged administration of either Banol (2-year feeding) or Mobam (1-year feeding) did not change the serum or liver β-Glu activities, although red cell ChE was inhibited at 500 and 1000 ppm levels of Mobam. Single doses of parathion given to rats fed diets of varying casein content markedly elevated serum β-Glu activity at all protein levels; the greatest increase (800-fold) appeared at the 15% casein level 2.5 hours after parathion injection. Aldrin or chlordane given at levels which stimulated serum and liver aliesterases, and triethyltin, coumarin, or dihydrocoumarin given at levels causing no macroscopic liver changes, did not affect serum or liver β-Glu activities.

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