Evidence for the involvement of μ-opioid and δ-opioid receptors in the antinociceptive effect caused by oral administration of m-trifluoromethyl-diphenyl diselenide in mice.

Pain is one of the most prevalent conditions, which limits productivity and diminishes quality of life. This study examined the antinociceptive effects of m-trifluoromethyl-diphenyl diselenide [(m-CF3-C6H4Se)2] on behavioral models of pain in mice. The involvement of opioid receptors in (m-CF3-C6H4Se)2-induced antinociception was evaluated in the tail-immersion test. (m-CF3-C6H4Se)2 exhibited significant inhibition of nociception induced by capsaicin (1.6 μg/paw, intraplantarly) (10-100 mg/kg, orally), and acetic acid (1.6%, 10 ml/kg, intraperitoneally) (1-100 mg/kg, orally), and in tail-immersion (50-100 mg/kg) and hot-plate (10-100 mg/kg) tests. The antinociception caused by (m-CF3-C6H4Se)2 in the tail-immersion test was significantly attenuated by naloxone (a nonselective opioid antagonist, 1 mg/kg, subcutaneously), naloxonazine (a selective μ-opioid receptor antagonist, 35 mg/kg, subcutaneously), or naltrindole (a selective δ-opioid receptor antagonist, 5 mg/kg, intraperitoneally). In contrast, (m-CF3-C6H4Se)2-induced antinociception was not affected by treatment with nor-binaltorphimine (a selective κ-opioid receptor antagonist, 10 mg/kg, subcutaneously) or naloxone methiodide (a peripherally restricted opioid antagonist, 1 mg/kg, subcutaneously). These results indicate that (m-CF3-C6H4Se)2-elicited antinociception in different models of pain through mechanisms that seem to involve an interaction with the central opioid system, more specifically μ-opioid and δ-opioid receptors.