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Interestingly, although PCTX does not cause direct mitochondrial DNA damage, mitochondria have been suggested as potential mediators for PCTX toxicity, as swollen and vacuolated mitochondria have been observed in myelinated and unmyelinated sensory nerves, thus the authors conclude that alterations in mitochondria contribute to PCTX-induced pain instead of dysfunctions of axonal microtubules (Flatters and Bennett 2006
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