Abstract
Objective The effects of lead exposure on cognitive function have been studied intensively over the past decade, but less attention has focused on its impact on auditory function. This study is aimed at investigating the effect of lead on the cochlea and the molecular mechanisms responsible for its actions. Methods 0.2% lead acetate was administered to rats in drinking water for 30, 60, and 90 days. Brainstem auditory evoked responses (ABR) were recorded, and morphological changes in the hair cells were observed. We also measured glutathione (GSH) and malondialdehyde (MDA) concentrations and antioxidant enzyme activities such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione reductase (GR) activities in the cochlea. Results Lead exposure increased the ABR threshold and slightly prolonged the latencies of wave II and wave IV in rats. Abnormally shaped hair cells and loss of hair cells were found in the cochlea basilar membrane, together with degenerative changes in spiral ganglion neurons following lead exposure. The activities of some antioxidant enzymes were also reduced in association with upregulation of MDA expression. These effects may be caused by impaired catalytic function of the enzymes as a result of lead interaction. Conclusion The antioxidant system of the cochlea in the immature rat brain is highly vulnerable to developmental lead exposure. Oxidative stress may therefore represent a possible mechanism for lead-induced auditory deficits.
Highlights
Lead is one of the most widespread and insidious environmental toxins and is primarily derived from human activities and from a variety of products such as paints, cosmetics, building materials, gasoline additives, and water pipes [1]
Previous studies in humans and experimental animals clearly indicated that lead exposure could result in ototoxicity, including electrophysiological changes in the cochlea and hearing loss; the mechanisms underlying the toxic effects of lead on the auditory system remain largely unknown
The results of the present study clearly demonstrate that auditory function in rats was impaired following lead exposure
Summary
Lead is one of the most widespread and insidious environmental toxins and is primarily derived from human activities and from a variety of products such as paints, cosmetics, building materials, gasoline additives, and water pipes [1]. Lead exposure was previously shown to be a highrisk factor for auditory system disturbances [8], with potentially more severe auditory implications than noise exposure [9]. Previous studies showed that lead exposure increased hearing thresholds [13, 14], the latency of the auditory brainstem response [11, 15], and the auditory nerve action potential threshold [16]; altered the axonal integrity and myelin organization within the cochlear nerve, brainstem auditory nuclei, and white matter [16,17,18]; and reduced glucose metabolism in several auditory centers [19]. Lead can penetrate the blood-brain barrier and act directly on the neurons of the auditory center by injuring astrocytes and the endothelial microvasculature [20]. The impact of lead exposure on the cochlea and its mechanisms of action remain poorly understood
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