Cell cycle disruption and apoptosis as mechanisms of toxicity of organochlorines in Zea mays roots.

Organochlorine pesticides (OCPs) are widespread environmental pollutants; two of them are highly persistent: lindane (γHCH) and chlordecone (CLD). Maize plants cope with high levels of OCP-environmental pollution, however little is known about cellular mechanisms involved in plant response to such OCP-exposures. This research was aimed at understanding the physiological pathways involved in the plant response to OCPs in function of a gradient of exposure. Here we provide the evidences that OCPs might disrupt root cell cycle leading to a rise in the level of polyploidy possibly through mechanisms of endoreduplication. In addition, low-to-high doses of γHCH were able to induce an accumulation of H2O2 without modifying NO contents, while CLD modulated neither H2O2 nor NO production. [Ca(2+)]cytosolic, the caspase-3-like activity as well as TUNEL-positive nuclei and IP-positive cells increased after exposure to low-to-high doses of OCPs. These data strongly suggest a cascade mechanism of the OCP-induced toxic effect, notably with an increase in [Ca(2+)]cytosolic and caspase-3-like activity, suggesting the activation of programmed cell death pathway.
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