Journal of

Introduction: Influences of lead on functions of many organ systems are known, but less experimental studies has been done on influences over the behavior, including pain sensation. This study was carried out to reveal possible changes in the onset and intensity of reactions to painful stimuli in mice, after long-term exposure to lead acetate.

Methods: In this experimental study, 24 adult male albino mice were divided randomly into 3 groups of 8 each. Control group received fresh water ad lib and 2 treated groups received drinking water contaminated by either 5 ppm or 500 ppm of LA for 90 consecutive days. On the day of 91, nociceptive were performed using a hot plate and formalin, to evaluate onset and intensity of  reaction in response to the thermal and chemical pain, respectively. At the end, the animals were euthanized and blood samples were collected for determination of cortisol levels using an ELISA assay.

Results: The animals exposed to LA showed a delay in reaction to painful stimuli induced by thermal stimulus by 52% and 59% with low and high doses, respectively. Thermal pain intensity of reactions to was declined by 63% with LA 5 ppm and by 82% with LA 500 ppm (P<0.05). Delayed reaction to chemical stimulus was also prominent in treated groups up to 68% and the pain intensity was declined by 80%, but they were not statistically significant. Blood cortisol levels remained almost unchanged.

Conclusion: Delayed reaction to painful stimuli after chronic LA exposure may be considered as a complication which weaken the alarming role of the pain. Further studies regarding the mechanism of action and the extent of the importance of these effects are warranted.