Toxicology and applied pharmacology
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Toxicol. Appl. Pharmacol. · Feb 1986
The developmental toxicity of xylene and xylene isomers in the Hydra assay.
Two laboratories tested multiple forms of xylene for their developmental toxicity hazard potential (A/D ratio) by means of the hydra assay. The three isomers, as well as a solution of mixed xylenes, all interfered with development (D) at or near to concentrations that also were toxic to adult (A) hydra. ⋯ In each instance every xylene tested interfered with the same stage or developmental sequence and in a concentration-related manner. The hydra assay may be useful for establishing priorities to test agents in a more elaborate system, but substances less soluble than xylene may exceed the test's applicability.
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Toxicol. Appl. Pharmacol. · Dec 1985
Comparative StudyComparative sensitivity of bovine and rodent acetylcholinesterase to in vitro inhibition by organophosphate insecticides.
Biochemical studies were conducted to compare the in vitro sensitivities of bovine and rodent brain and erythrocyte cholinesterases to inhibition by Dyfonate-oxon, paraoxon, and malaoxon. This comparison was done to determine if the reported greater sensitivity of cattle to Dyfonate might be explained by a greater sensitivity of the target enzyme, acetylcholinesterase, in cattle to inhibition by Dyfonate's toxic metabolite, Dyfonate-oxon. Studies were conducted with brain homogenates and lysed erythrocytes obtained from cows and from male and female rats. ⋯ This study demonstrated that, as an inhibitor of ACHE in vitro, Dyfonate-oxon was equal to or slightly lower in potency than paraoxon and more potent than malaoxon. In addition, the study demonstrated that, in general, ACHE from brain or erythrocytes of cows was less sensitive to in vitro inhibition by organophosphates than was that from male or female rats. Thus, the apparent greater susceptibility of cows to Dyfonate, in vivo, cannot be explained on the basis of an unusual target enzyme (ACHE) sensitivity to inhibition by Dyfonate-oxon.
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Toxicol. Appl. Pharmacol. · Sep 1983
Amelioration of mercuric chloride-induced acute renal failure by dithiothreitol.
Experiments were conducted to determine if administration of the sulfhydryl reducing agent and metal chelator dithiothreitol (31 mg/kg body wt) alters the development of renal dysfunction in the first 3 hr after injection of mercuric chloride (3 mg/kg). Mercuric chloride alone resulted in elevation of urine flow rate and fractional excretion of solutes within 30 min of injection. In animals injected with dithiothreitol 60 min after mercuric chloride, urine flow rate and fractional excretion of solutes were reduced within 30 min to values intermediate between control and mercuric chloride-treated rats. ⋯ Measurement of mercury in organs of those rats injected with mercuric chloride alone or prior to dithiothreitol revealed no alteration in organ distribution. The renal cortex contained the highest concentrations of mercury, and these concentrations were comparable in both groups of rats. These studies demonstrate that dithiothreitol can ameliorate the renal toxicity of mercury and suggest that this effect is mediated through an intrarenal site of action.