Response of five species of stored‐product insects to phosphine in oxygen‐deficient atmospheres

Abstract

Five species of stored‐product insects, [Tribolium castaneum (Herbst), T. confusum (DuVal), Rhyzopertha dominica (F.), Sitophilus oryzae (L.) and S. granarius (L.)], exposed to phosphine in nitrogen and various oxygen‐deficient atmospheres, showed reduced susceptibility to three concentrations of phosphine (0.02, 0.04 and 0.2 mg litre−1). The last two species also showed reduced susceptibility to phosphine at 2.0 mg litre−1. Generally mortality increased progressively as the level of oxygen was raised. There was a close relationship between the ability of insects to withstand anoxia and survival from phosphine treatment.

Effect of acute aluminum phosphide exposure on rats—A biochemical and histological correlation

“…Phosphine has been shown to inhibit respiration in insects Price and Dance, 1983), intact nematodes and mitochondria of rat liver (Dua et al, 2010b;Nakakita et al, 1971). A direct correlation was also observed between the degree of suppression and mitochondrial respiration; living organisms were not affected when exposed to phosphine under hypoxic conditions (Kashi, 1981) conversely, hyperoxic conditions (Cheng et al, 2003) and mitochondrial uncouplers (Valmas et al, 2008) increased sensitivity. Evidences also show a decrease in mitochondrial oxygen consumption, ATP levels, synthesis and hydrolysis (Dua et al, 2010b) culminating in a metabolic and energy crisis (Dua et al, 2010a;Zuryn et al, 2008).…”

The interaction of phosphine with haemoglobin and erythrocytes

“…In insects the acute toxic action of phosphine is dependent on oxygen (Bond et al 1967, Kashi 1981, and a number of studies have demonstrated that phosphine is a respiratory poison for insects (Cherfurka et al 1976, Kashi 1981. A significant biochemical target for phosphine is cytochrome oxidase in mitochondria (Price and Dance 1983), although when insects were treated with lethal doses of phosphine, their cytochrome oxidase was inhibited by no more than SO%, indicating that inhibition of this enzyme was not directly responsible for the mortality (Nakakita 1987).…”

Caenorhabditis elegans Mutants Resistant to Phosphine Toxicity Show Increased Longevity and Cross-Resistance to the Synergistic Action of Oxygen

“…Chaudhry and Price (1990) have combined these two features in a model which proposes that electron donation by phosphine is facilitated by its interaction with transition metals, such as iron. In addition, phosphine toxicity is absolutely dependent on oxygen (Kashi, 1981). However, the nature of a potential interaction between phosphine, transition metals, and oxygen in vivo is completely unknown.…”