Smoking has been positively associated with hearing loss in human. However, its effect on the cochlea has not been previously evaluated. Aim of work is to investigate the effect of nicotine, which is the primary pharmacological component of tobacco, on the structure of the cochlea of adult male guinea pigs. Fifteen male guinea pigs were classified into two groups: group I (control) and group II (nicotine treated group). Group II was further subdivided into two subgroups; IIA and IIB according to the dose of nicotine (3 mg/kg and 6 mg/kg, respectively). The cochlea was harvested and processed for light microscopy, transmission electron microscopy and scanning electron microscopy. Nicotine administration induced damage of outer hair cells which were distorted in shape with vacuolated cytoplasm and heterochromatic nuclei. Topography revealed damage of the stereocilia which included disorganization, bent and limp or complete loss and expansion of the surrounding supporting cells. These changes were more pronounced in the basal turn of the cochlea and mainly involved the outer hair cells. High dose induced more damage and resulted in protrusion of the apical poles of hair cells (blebing), particularly the outer two rows. Nicotine is proved to be harmful to the cells of the cochlea, particularly the outer hair cells of the basal turn. High doses induce blebing of hair cells.

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Limb ischemia reperfusion (I/R) injury is associated with serious local and systemic effects. Reperfusion may augment tissue injury in excess of that produced by ischemia alone. The hippocampus has been reported to be vulnerable to I/R injury. Alpha lipoic acid (ALA) is an endogenous antioxidant with a powerful antioxidative, anti-inflammatory, and antiapoptotic properties. We studied the probable restorative effect of ALA on limb I/R-induced structural damage of rat hippocampus. Forty adult male albino rats were divided equally into four groups: group I (sham); group II (I/R-1 day) has undergone bilateral femoral arteries occlusion (3 h), then reperfusion for 1 day; group III (I/R-7 days) has undergone reperfusion for seven days; group IV (I/R-ALA) has undergone I/R as group III and received an intraperitoneal injection of ALA (100 mg/kg) for 7 days. I/R groups revealed degenerative changes in the pyramidal neuronal perikarya of CA3 field in the form of dark-stained cytoplasm, dilated RER cisternae, mitochondrial alterations, and dense bodies' accumulation. Their dendrites showed disorganized microtubules. Astrogliosis is featured by an increased number and increased immunoreactivity of astrocytes for glial fibrillary acid protein. Morphometric data revealed significant reduction of light neurons, surface area of neurons, and thickness of the CA3 layer. Most blood capillaries exhibited narrow lumen and irregular basal lamina. ALA ameliorated the neuronal damage. Pyramidal neurons revealed preservation of normal structure. Significant increase in the thickness of pyramidal layer in CA3 field and surface area and number of light neurons was observed but astrogliosis persisted. Limb I/R had a deleterious remote effect on the hippocampus aggravated with longer period of reperfusion. This work may encourage the use of ALA in the critical clinical settings with I/R injury.

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