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J S Bus

Publications and source records attributed to J S Bus.

66 records · Page 4Linked to original sources
PubMed1976

Effect of paraquat (methyl viologen) on liver function in mice.

Paraquat poisoning may result in pulmonary damage and hepatotoxicity. To examine the effect of paraquat on liver function, paraquat-treated mice were injected with sulfobromophthalein (BSP, 100 mg/kg) or indocyanine green (20 mg/kg) via the tail vein and plasma concentrations of these compounds were determined at various times. Hepatic concentrations of reduced glutathione were also determined following paraquat. Retention of BSP and indocyanine green in the plasma was observed 24 hours after paraquat. Body temperature of the poisoned mice was significantly depressed 24 hours after treatment and the paraquat-induced indocyanine green retention could be reversed by warming the paraquat-treated mice to normal body temperature. In contrast, paraquat-induced BSP retention was independent of body temperature. Inasmuch as hepatic glutathione concentrations were reduced 24 hours after paraquat treatment, the retention of BSP in the plasma may have been secondary to the reduction of hepatic glutathione concentrations.

Animals↗
PubMed1975

Lipid peroxidation: a possible mechanism for paraquat toxicity.

The toxicity of the herbicide paraquat in mice, measured by the single dose lethal to 50 per cent of the animals after 7 days, was significantly enhanced by prior exposure to diets deficient in selenium or vitamin E and by pretreatment with diethyl maleate. These data suggest lipid peroxidation to be an important in vivo biochemical mechanism of paraquat toxicity as both selenium and vitamin E have antioxidant functions.

Animals↗
PubMedDate not supplied

Studies on the renal transport of trimethylpentanoic acid metabolites of 2,2,4-trimethylpentane in rat renal cortical slices.

2,2,4-Trimethylpentane (TMP), a nephrotoxic component of unleaded gasoline in male but not female rats, undergoes oxidative metabolism to yield 2,2,4- and 2,4,4-trimethylpentanol, pentanoic acid and 5-hydroxypentanoic acid. We have examined the effect of three of these pentanoic acid metabolites on the renal transport of the organic anion p-aminohippurate (PAH) and the organic cation tetraethylammonium (TEA) in renal cortical slices from male Fischer 344 rats. 2,4,4-Trimethylpentanoic acid, the major urinary metabolite in rats, produced a selective decrease in the accumulation of PAH without affecting TEA accumulation. Kinetic analysis showed that 2,4,4-trimethylpentanoic acid was a competitive inhibitor of the organic anion transport system, with a Ki of 4 mM. 2,4,4-Trimethyl-5-hydroxypentanoic acid also showed selective inhibition of PAH transport, while 2,2,4-trimethylpentanoic acid was less selective and reduced both PAH and TEA transport. Additional studies with radiolabeled 2,4,4-trimethylpentanoic acid showed that there was a time- and concentration-dependent accumulation of radioactivity into slices of renal cortex. However, experiments conducted at 4 degrees C and studies with metabolic inhibitors, or with an inhibitor of organic anion transport, indicated that little of the accumulated material was entering the cell. We conclude from these studies that the pentanoic acid metabolites formed from 2,2,4-trimethylpentane are not actively transported by the renal organic anion transport system. In summary, in vitro the pentanoic acid metabolites appear to bind to renal cortical tissue and thereby reduce the transport of PAH.

Animals↗
PubMedDate not supplied

Dose-dependent disposition of n-hexane in F-344 rats after inhalation exposure.

The purpose of this study was to assess the disposition of radioactivity in rats after single inhalation exposures to varying concentrations of [1,2-14C]-n-hexane. Male Fischer 344 rats were exposed to 500, 1000, 3000 or 10,000 ppm 14C-n-hexane for 6 hr and the elimination of radioactivity followed for 72 hr after exposure. The disposition of radioactivity was dose-dependent, with 12, 24, 38 and 62% of the acquired body burden excreted as n-hexane by the lung with increasing exposure concentration. In contrast, 38, 31, 27 and 18% of the body burden of radioactivity was recovered as expired 14CO2 and 35, 40, 31 and 18% was recovered in the urine with increasing n-hexane concentration. Radioactivity remaining in the tissues and carcass 72 hr after exposure represented 6.1, 8.8, 7.4 and 5.4% of the body burden for the respective exposures. The dose-dependent elimination of radioactivity was apparently due in part to an inhibition of n-hexane metabolism, reflected by a decrease in total 14CO2 and urinary 14C excretion after 10,000 ppm exposure compared to the 3000 ppm exposure.

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