Role of acetylcholinesterase and glutathione S-transferase following exposure to nicosulfuron and diazinon in Helicoverpa zea.

The acute toxicity of diazinon combined with the herbicide nicosulfuron was determined using the corn earworm, Helicoverpa zea. Nicosulfuron significantly increased toxicity of diazinon to H. zea compared to diazinon alone based on dip bioassays to evaluate acute contact toxicity. Diazinon, an organophosphorous insecticide, controls insects by inhibiting acetylcholinesterase in the nervous system. Acetylcholinesterase activity was significantly altered in corn earworms exposed to binary mixtures compared to those exposed to diazinon alone; however, the activity did not correspond consistently with toxicity. Glutathione S-transferase (GST), also known to be altered by organophosphorous insecticides, did not exhibit significant changes following exposures to diazinon, nicosulfuron, or binary mixtures. Our results suggest that nicosulfuron increases toxicity of diazinon but the mechanism of toxicity does not appear to be correlated with acetylcholinesterase or GST inhibition.

Lead-induced alterations of apoptosis and neurotrophic factor mRNA in the developing rat cortex, hippocampus, and cerebellum.

Previous reports have recently shown the prototypic neurotoxicant, lead, to induce apoptosis in the brains of developing organisms. In the current study, timed-pregnant rats were exposed to lead acetate (0.2% in the drinking water) 24 h following birth at postnatal day 1 (PND 1). Dams and pups were continuously exposed to lead through the drinking water of the dam until PND 20. Postnatal exposure in the pups resulted in altered mRNA levels of the following apoptotic and neurotrophic factors: caspase 2 and 3, bax, bcl-x, brain-derived neurotrophic factor (BDNF). Ribonuclease protection assays were conducted to measure the factors simultaneously at the following postnatal time points: 9, 12, 15, 20, 25, days. Our results suggest a brain region- and time-specific response following lead acetate exposure. The region most vulnerable to alterations occurs in the hippocampus with alterations beginning at PND 12, in which caspase 3, bcl-x, BDNF increase with lead exposure. Significant treatment effects were not observed for both the cortex and cerebellum.