THE EFFECT OF COBALT CHLORIDE PRECONDITIONING ON PACLITAXEL-INDUCED PERIPHERAL NEUROPATHY

Recent studies indicate that Cobalt Chloride (CoC12) modulates mitochondrial activity. There is emerging data suggesting that Paclitaxel-induced peripheral neuropathy (PIPN) is a consequence of the drug's mitochondrial toxicity.

to assess the effect of CoC12 preconditioning on PIPN in an animal model.

PIPN was induced by 7 daily consecutive i.p. Paclitaxel (PXT) administrations. Male BALB/c mice were divided into three groups as follows: group A--CoC12 (12.5 mg/kg b.w.) for three weeks (preconditioning) followed by I week of PXT, group B--saline for three weeks, followed by 1 week of PXT and group C--saline for four weeks. Thermal and mechanical allodynia were assessed by means of paw withdrawal latency (PWL).

In group A, CoC12 preconditioning lead to a decrease in both thermal and mechanical PWLs. 7 days after the last dose of PXT, however, values returned to normal in group A and allodynia for both thermal and mechanical stimuli was noted in group B (p < 0.05).

CoC12 preconditioning seems to protect against PIPN. Although CoC12 administration decreased thermal and mechanical PWLs, subsequent P administration did not lead to the persistent mechanical and thermal allodynia that was noted in the P-alone group. Further studies are required for determining the exact relationship between CoC12 and PIPN.