Indol-3-ylacetic acid- and calmodulin-regulated Ca2+-ATPase: A target for the phytotoxic action of hexachlorocyclohexane

In rice seedlings, the organochlorine insecticide hexachlorocyclohexane (HCH) and its four major isomers—α,β, γ, and δ—have been shown to elicit their phytotoxic action by interacting with indol-3-ylacetic acid (IAA)-regulated growth and Ca²⁺-ATPase activity. When rice seedlings were grown in the presence of 0.34 mM HCH, seedling vigour was reduced to 33% of the control. A similar effect was observed when seedlings were grown in the presence of the γ and δ isomers, but not with the α and δ isomers of HCH. This reduced vigour could be restored by treating the seedlings with 100 nM IAA, suggesting that HCH and its isomers (γ and δ) limit either IAA synthesis or action or both. In a microsomal fraction from rice seedlings grown in the presence of either HCH or its isomers, the calmodulin-regulated Ca²⁺-ATPase activity was inhibited as follows: technical HCH = 46%, α isomer = 80%, β isomer = 72%, γ isomer = 65% and δ isomer = 62% of the control value, respectively. TLC analysis suggested that the various isomers of HCH are metabolised by the plant, except for the δ isotner, which accumulated. This isomer, along with the degraded products of other isomers, may be responsible for the phytotoxic action of HCH.