Melatonin and sciatic nerve injury repair: a current perspective

Berrin Zuhal Altunkaynak,1 Burcu Delibaş,2 Gamze Altun,2 Ömür Gülsüm Deniz2 1Department of Histology and Embryology, Medical Faculty, Okan University, Istanbul; Turkey; 2Department of Histology and Embryology, Medical Faculty, Ondokuz Mayıs University, Samsun, Turkey Abstract: Peripheral nerve injury is an important clinical problem that can exert hazardous effects on the health of patients. For this reason, there are more studies conducted on the regeneration of the peripheral nerves via the usage of the nerves belonging to various animals with different types of lesions, ages, and by using different methods of assessment with regular follow-up. Contrary to data obtained through experimentation and clinical observation, no ideal way of treatment was found to increase the regeneration of the peripheral nerves. Finally, the effects of melatonin in the protection of peripheral nerves against trauma, especially the protection of sciatic nerve from pathological conditions, have come into attention in a wide group of scientists as there are beneficial effects of melatonin after surgery. While numerous studies indicate the melatonin’s protective effects on the pathologies of nerves, there are also studies reporting its toxic effects on peripheral nerves. Melatonin is a widespread and crucial signaling molecule due to its features of free radical scavenging and anti-oxidation at both pharmacological and physiological conditions in vivo. In this context, although there are numerous studies elaborating the effects of melatonin in various tissues, its effects on peripheral nerves was documented in only a limited number of studies. The aim of this article was to perform a review of the knowledge in the literature on the subject of mostly beneficial or hazardous effects of melatonin on the repair of the damaged peripheral nerves. Keywords: peripheral nerve injury, melatonin, regeneration, light and electron microscop

A stereological study of the effects of mercury inhalation on the cerebellum.

Mercury in the environment that arises from organic and inorganic sources can cause irreversible damage to the nervous system. Toxicity may be direct or may arise from interactions with other metals in the environment. We evaluated the possible effects of mercury vapor on rat cerebellum. Twelve adult female rats were divided into control and experimental groups. The rats in the experimental group were exposed to mercury vapor for 9 h/day for 45 days. Cerebellar tissue samples were evaluated using stereology and for histopathology. The total number of Purkinje cells was estimated using a physical disector method. We found that in the experimental group, overall volume decreased and the number of Purkinje cells was reduced. We also found cellular damage including pycnotic nuclei, eosinophilic cytoplasm and vacuolization; these features were absent in the control group. We found that chronic exposure to inorganic mercury vapor is toxic to the cerebellum

The effects of high-fat diet on the renal structure and morphometric parametric of kidneys in rats

To characterize the kidney in a high-fat-induced obesity model, we examined the renal structure of adult Sprague–Dawley rats fed a control diet or a high-fat diet for 3 months. Ten adult female Sprague–Dawley rats were fed a diet consisting highly of fat (30%) for a period of 3 months. Ten control rats were maintained with standard rat chow. All animals were weighed every 10 days for 3 months. At the end of the experiment, the naso-anal length of the anaesthetized rats was measured to calculate body mass index, and subsequently whole kidneys of intracardially formalin-perfused animals were removed. Quantitative features of the kidney were analysed with the Cavalieri and physical dissector methods applied to serial paraffin sections. Kidney samples were also examined histologically. The body mass indices of the control and treatment groups were 4.528 ± 0.242 and 5.876 ± 0.318 kg m−2, respectively. The difference between the body mass indices of the two groups was statistically significant (P < 0.01, Mann–Whitney U-test), suggesting that the animals fed with a high-fat diet may be overweight. Stereological examination of the kidneys revealed differences in kidney weight, total kidney volume, volume of cortex, medulla, glomeruli, proximal and distal tubules, and numerical density of glomeruli and glomerular height in the treatment group compared with the control group. Light microscopic investigation showed a dilatation in blood vessels and Bowman's space, mononuclear cell infiltration, degeneration in nephrons, including glomerulosclerosis and tubular defects, and an increase in the connective tissue in the kidneys in the treatment group. We concluded that a fatty diet is responsible for the rats’ obesity and may lead to renal deformities as a result of histopathological changes such as dilatation, tubular defects, inflammation and connective tissue enlargement of the kidney