Potentiation of Toxicity of Malathion by Triorthotolyl Phosphate.

Abstract

483gest that this approach would produce data more reliable than red cell uptake of radioiron, especially during weak or short-lived effects. Hodgson et aZ. (12) have reached the same conclusion following use of this method to study bone marrow stimulation. These experiments are being extended to determine the limits of accuracy and sensitivity of this method.We studied the depression of plasma radioiron turnover rates in rats following X-irradiation. The depression is prompt (maximal by 24-30 hours) and, at 24 hours post-irradiation, is directly related to dose between 50 r and 300 r. Recovery occurs by the 6th post irradiation day, indicating that subsequent anemia is more likely due to hemorrhagic diathesis than bone marrow dysfunction. Sensitivity of the radioiron turnover method permitted a study of bone marrow response at frequent short intervals after irradiation. Summary.We gratefully acknowledge technical assistance of Mr. Alfred E. Seaton.1. Jacobson, Leon 0.

Dose and Time Determining, and Other Factors Influencing, Toxicity

“…A factor greater than 100 was found for potentiation between malathion and triorthocresyl phosphate (TCP) (Murphy et al, 1959). Although TCP is an organic phos phorus compound, it is not a pesticide.…”

Anticholinesterase Pesticides Interactions

“…The marked synergism of malathion þ BPMC could not be explained on the basis of an inhibition of AChE by malaoxon þ BPMC, or an inhibition of malathion's detoxication by BPMC. In previous studies, the synergism of malathion toxicity by EPN or tri-o-cresyl phosphate (TOCP) has been extensively studied and explained by the inhibition of CarbE, which hydrolytically detoxifies malathion and malaoxon (Cohen et al, 1972;Murphy et al, 1959). However, the marked synergism of malathion þ BPMC could not be explained by the inhibition of malathion's detoxication by BPMC, because the activity of CarbE was not inhibited after administration of BPMC.…”

“…For example, malathion, which contains a carboxylic ester linkage, is hydrolytically detoxified by tissue CarbEs and is markedly potentiated by other OP agents that inhibit the esterases (Cohen, 1984;Frawley et al, 1957;Murphy et al, 1959;Seume and O'Brien, 1960). However, inhibition of CarbEs was not observed after BPMC administration (Takahashi et al, 1983).…”

“…Since the 1950s there have been a number of studies on the combined acute toxicity of OP compounds following simultaneous or sequential Anticholinesterase Pesticides: Metabolism, Neurotoxicity, and Epidemiology. Edited by Tetsuo Satoh and Ramesh C. Gupta Copyright # 2010 John Wiley & Sons, Inc. administration (DuBois, 1961;Murphy, 1969Murphy, , 1980Murphy et al, 1959). In most studies, these compounds were administered in various combinations in laboratory animals, including dogs, to assess the resulting effect (additive, potentiation/synergistic, or antagonistic).…”

Mutagenic efficiency of organophosphorus insecticides used in combined treatments.

“…The potentiation of anticholinesterase action is explained by the inhibition of carboxyesterase and carboxyamidase which detoxify the pesticides. The first compound competes with the detoxifying enzyme, impeding hydrolysis of the other, which results in a protracted action (3). These properties explain the increasing number of complex commercial insecticides which contain more than one active substance.…”