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ToxSci Advance Access published online on April 15, 2003
Toxicological Sciences, doi:10.1093/toxsci/kfg049
Toxicological Sciences © Society of Toxicology 2003; all rights reserved
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Received October 2, 2002; accepted January 23, 2003
© 2003 Society of Toxicology

Environmental Toxicology

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

Qiang Cheng 1, Nicholas Valmas 1, Paul E. B. Reilly 1, Patrick J. Collins 2, Rosemary Kopittke 2, Paul R. Ebert 1*

1 Department of Biochemistry and Molecular Biology, The University of Queensland, St Lucia, QLD 4072 Australia
2 Queensland Department of Primary Industries, 80 Meiers Road, Indooroopilly, QLD 4068 Australia

* To whom correspondence should be addressed. E-mail: p.ebert{at}uq.edu.au.


  Abstract

Phosphine (hydrogen phosphide, PH3) is the fumigant most widely used to protect stored products from pest infestation. Despite the importance of this chemical, little is known about its mode of action. We have created three phosphine resistant lines (pre-1, pre-7, pre-33) in the model organism C. elegans, with LC50 values 2, 5 and 9 times greater than the fully susceptible parental strain. Molecular oxygen was shown to be an extremely effective synergist with phosphine as under hyperoxic conditions 100% mortality was observed in wild type nematodes exposed to 0.1 mg/l phosphine, a non-lethal concentration in air. All three mutants were resistant to the synergistic effects of oxygen in proportion to their resistance to phosphine with one mutant, pre-33, showing complete resistance to this synergism. We take the proportionality of cross-resistance between phosphine and the synergistic effect of oxygen to imply that all three mutants circumvent a mechanism of phosphine toxicity that is directly coupled to oxygen metabolism. Compared with the wild type strain, all three mutants have an extended average life expectancy from 12.5 to 25.3%. This is consistent with the proposed involvement of oxidative stress in both phosphine toxicity and ageing. Because the wild type and mutant nematodes develop at the same rate, the longevity is unlikely to be caused by a clk -type reduction in oxidative metabolism, a potential alternative mechanism of phosphine resistance.

methyl bromide, oxidative stress, oxygen toxicity, ROS, mitochondrial dysfunction, EMS mutagenesis, clk-1, insecticide, fumigant, hyperoxia .


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