Neurological impact of sub-chronic lead acetate exposure on pain perception in mice.

Abstract

Lead exposure is a significant environmental health concern with potential impacts on pain perception and physiological functions. This study investigates the effects of sub-chronic lead acetate exposure on pain threshold, pain intensity, blood cortisol levels, and metabolic parameters in 24 adult male albino mice. The mice were randomly divided into three groups: a control group that received fresh water and two experimental groups that received drinking water containing lead acetate at concentrations of 5 ppm and 500 ppm over a twelve-week period. Pain perception was assessed using thermal (hot plate test) and chemical (formalin injection) pain models. Exposure to lead acetate resulted in a significant increase in the latency to thermal pain response, with delays of 52 % in the 5 ppm group and 59 % in the 500 ppm group (P < 0.05). Thermal pain intensity was reduced significantly by 63 % in the 5 ppm group and 82 % in the 500 ppm group (P < 0.05). However, changes in the onset time and intensity of chemical pain, as well as blood cortisol levels, were not statistically significant. Additionally, no significant differences in food and water intake or body weight changes were observed among the groups. These findings indicate that lead exposure can alter pain perception, with effects most pronounced in the context of thermal pain. Future research should explore lead's impact across different age groups and developmental stages, as well as its effects on specific neurotransmitter systems and receptor interactions. This research provides insights into the complex effects of lead on neurological function and highlights the importance of understanding lead's broader physiological impacts.