Fenitrothion, an organophosphorous insecticide, impairs locomotory function and alters body temperatures in Sminthopsis macroura (Gould 1845) without reducing metabolic rates during running endurance and thermogenic performance tests.

Abstract

Endemic Australian mammal species are exposed to pesticides used for locust control as they occupy the same habitat as the target insect. The authors examined the impact of an ultra-low volume formulation of the organophosphorous insecticide fenitrothion (O,O-dimethyl-O-[3-methyl-4-nitrophenol]-phosphorothioate) on a suite of physiological measures that affect the ability of animals to survive in free-living conditions: locomotory and thermogenic functions, metabolic performance, body mass, and hematocrit and hemoglobin levels. Plasma and brain cholinesterase activity in relation to time since exposure to pesticide were also determined. An orally applied dose of 90 mg kg(-1) fenitrothion reduced running endurance in the stripe-faced dunnart, Sminthopsis macroura, by 80% the day after exposure concomitantly with a reduction of approximately 50% in plasma and 45% in brain acetylcholinesterase activity. These adverse effects disappeared by 10 d postexposure. Maximal metabolic rates reached during running were unaffected by pesticide, as were body mass and hemoglobin and hematocrit levels. Maximal cold-induced metabolic rate (measured as peak 2 min metabolic rate attained during cold exposure), time taken to reach peak metabolic rate on cold exposure, cumulative total oxygen consumed during shivering thermogenesis, and body temperature before and after cold exposure were unaffected by fenitrothion. Dunnart rectal temperatures showed a reduction of up to 5 °C after exposure to fenitrothion but returned to pre-exposure levels by 10 d postdose. Such physiological compromises in otherwise asymptomatic animals demonstrate the importance of considering performance-based measures in pesticide risk assessments.