Abstract
Noise, a disturbing and unwanted sound is currently being perceived as a widespread environmental stressor. In the present study we investigated the activation of oxidative stress as a mechanism involved in cognitive impairment through changes in neuro-inflammation. Sprague Dawley rats (200-220 g m) were exposed to moderate (100dB) sound pressure level (SPL) noise daily for 2 h s over a period of 15 and 30 days and the consequence on brain regions of hippocampus observed through behavioral studies by Morris Water Maze to assess effects on spatial memory coupled with biochemical evaluation of markers of oxidative stress and inflammation. Further, the underlying mechanism pertaining to apoptosis was investigated by immuno-histological studies through assessment of Caspase-3 and TUNEL assay as well as morphological parameters, namely Nissl bodies in CA1, CA3 and DG regions of hippocampus. Poorer performance in the MWM indicative of decrement in concept formation, attention, working memory, and reference memory was observed on 15 and 30 days of noise exposures. At the cellular level, increased oxidative stress and inflammation was noticed as evinced by elevated levels of TNF-α, IL-6, IL-1α and IFN-γ in both hippocampus and plasma. Exposure to noise also led to a gradual increase in the number of pyknotic and apoptotic neurons together with the increase in DNA fragmentation in hippocampus. Increased levels of inflammatory genes (i.g.) ccl2, ccr5, ifng, il13, il1a, tnfa coupled with decreased levels of bmp2 and il3 genes were found in both the noise exposure groups. Our findings revealed that moderate intensity noise exposure impaired early memory changes in expression of several gene families including genes associated with regulation of transcription, inflammatory response, and, response to oxidative stress.