This study aimed to assess the effects of nicotine on spermatogenesis in 140 mature male albino rats divided into group A (controls), group B (sham controls), group C (nicotine treated) and group D (nicotine withdrawal). Group C was subdivided into CI, CII, CIII according to the dose of injected nicotine (0.2, 0.4 and 0.6 mg nicotine per 100 g per day), where each subgroup was further subdivided according to the treatment duration into subgroups a, b and c that received nicotine for 2, 4 and 8 weeks. Group D received nicotine for 8 weeks followed by withdrawal for another 8 weeks to assess testicular recovery. Testicular tissue sections were subjected to haematoxylin and eosin, Masson's trichrome stains and morphometry. The results showed that nicotine caused degenerative changes in the seminiferous tubules, revealed by altered general tubular architecture, decreased thickness of the spermatogenic cell masses, Sertoli cell vacuolation and thickened basal lamina. These changes were proportional to the nicotine dose and duration. Following nicotine withdrawal, regeneration of the damaged seminiferous tubules was observed to be rather complete in CI group. It is concluded that nicotine could adversely affect testicular spermatogenesis in a dose- and time-dependent manner which would be almost reversible after nicotine withdrawal, especially after small doses.

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Our results suggested that administering silybin with polymyxin E alleviated polymyxin E-induced nephrotoxicity in the rat kidney. Future biochemical studies should investigate whether silybin could ameliorate the nephrotoxicity caused by polymyxin E in rats and whether concomitant administration of silybin could be an effective clinical pharmacological strategy to protect against polymyxin E-induced insult in human kidneys.

Rat retinae clearly undergo age-related morphological changes such changes provide a cellular base for explanation of decreased vision in humans with aging other than reflection errors. Effect of aging was not only qualitative, but also quantitative.

Acute restraint stress (ARS) is an unavoidable stress situation and may be encountered in different clinical situations. The aim of the current study was to investigate the effects of ARS on the hippocampus and cerebellum, assess the impact of these effects on the behavior and cognitive function, and determine whether pretreatment with ceftriaxone would attenuate the damages produced by ARS on the hippocampus and cerebellum. Four groups of male mice were included in this study: The control group, ARS group, ceftriaxone group, and ARS + ceftriaxone group. Tail suspension test, Y-maze task, and open field tests were used to assess depression, working spatial memory, and anxiety. The biochemical analyses included measurements of serum cortisol, tumor necrotic factor (TNF), interleukin-6, hippocampal expression of bone morphogenetic protein 9 (BMP9), lysosomal-associated membrane protein 1 (LAMP1), glutamate transporter 1 (GLT1), heat shock protein 90, cerebellar expression of S100 protein, glutamic acid decarboxylase (GAD), and carbon anhydrase. Histopathological examination of the brain sections was conducted on the hippocampus and cerebellum by hematoxylin and eosin stains in addition to ultrastructure evaluation using electron microscopy. Our results suggested that ceftriaxone had neuroprotective properties by attenuating the effects of ARS on the hippocampus and cerebellum in mice. This effect was demonstrated by the improvement in the cognitive and behavioral tests as well as by the preservation of the hippocampal and cerebellar architecture.