Persistence behavior of chlorpyrifos and biological toxicity mechanism to cucumbers under greenhouse conditions.

Chlorpyrifos, a broadly utilized insecticide, inhibits many cellular and physiological processes in plants. Here, the phyto-toxicity of chlorpyrifos on cucumber plants, as well as the dissipation kinetics of chlorpyrifos in leaves, were investigated. Those results showed that chlorpyrifos accumulated primarily in the leaves under normal agrochemical spraying conditions with the half-lives among 2.48-4.59 days. Residues of the primary metabolite, 3,5,6-trichloro-2-pyridinol (TCP), rapidly accumulated in plant tissues and soil with chlorpyrifos degradation. The application amount of chlorpyrifos had a significant effect on the persistence of chlorpyrifos and TCP in both plant and soil environments. Chlorpyrifos generated excessive reactive oxygen species (ROS) and malondialdehyde (MDA), which led to oxidative damage. High chlorpyrifos stress even inhibited antioxidant enzymes. The photosynthetic system and gas exchange were suppressed, which ultimately lead to inefficient light use under chlorpyrifos stress. Morphological results revealed that chlorpyrifos induced membrane damage and harmed organelles such as mitochondria and chloroplast. Noninvasive micro-test technology (NMT) showed that chlorpyrifos promoted intracellular Ca influx and efflux of H and K. The Ca influx was significantly stimulated after both high and low chlorpyrifos treatment with the minimum value of - 336.33 pmol·cm·s at 258 s and - 155.68 pmol·cm·s at 288 s, respectively. Chlorpyrifos stress reversed the H influx to an efflux in cucumber mesophyll with the mean value of 0.45 ± 0.03 pmol·cm·s and 0.19 ± 0.03 pmol·cm·s in cucumber plants under low and high chlorpyrifos stress. High chlorpyrifos stress dramatically increase K efflux in cucumber leaves by 13.68 times higher than the control. We suggest that ion homeostasis destruction, accompanied by ROS, resulted in oxidative damage to the mesophyll cell of cucumber seedlings.