Mitochondria response to camptothecin and hydroxycamptothecine-induced apoptosis in Spodoptera exigua cells

- Mitochondrial responses in CPTs induced apoptosis were investigated.
- Mitochondria exhibited change in morphology, distribution and ultrastructure.
- Increased cytosolic Ca2 +, disrupted MMP and released cytochrome c were observed.
- The mitochondrial pathway involves in IOZCAS-Spex-II cell apoptosis induced by CPT.

Camptothecin (CPT), a natural alkaloid extracted from Camptotheca acuminata Decne, exhibits potential insecticidal activities against various insect species. Our previous studies have showed that CPTs induced apoptosis in Spodoptera exigua Hübner cell line which is mediated preliminarily by the mitochondrial pathway. In this study, changes of mitochondrial morphologic and function were investigated to characterize mitochondrial responses in CPTs induced apoptosis. After incubation IOZCAS-Spex-II cells with CPT and HCPT, mitochondria exhibited obvious changes in the size, morphology and distribution, and ultrastructural alterations characterized by disruption of cristae and membrane. The typical characteristics of apoptosis, including chromatin condensation, nucleus shrivels, and cytoplasmic vacuoles were found. CPT and HCPT induced IOZCAS-Spex-II cell apoptosis accompanied with increased dramatically cytosolic Ca2 + and reduced mitochondrial membrane potential in the dose and time-dependent pattern. Cytochrome c release induced by CPT and HCPT was partially reduced in the presence of CsA, which suggested that the opening of mitochondrial permeability transition pore. Taken together, these results suggested the role of mitochondria in regulation of insect cell apoptosis, which provided the basic information for illustrating the apoptosis pathway in insects and for using reasonably CPTs to control insect pests.

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