The ameliorative effects of vinpocetine on apoptosis and HSP-70 expression in testicular torsion in rats.

Vinpocetine is a potent antioxidant and free radical scavenger. We investigated the effects of vinpocetine on torsion/detorsion (T/D) induced testicular damage, HSP-70 expression and germ cell apoptosis in rats. Sixty Wistar albino adult male rats were divided into five groups of 12. The groups comprised a control group, a sham treated group, a T/D group, a vinpocetine treated group, and a T/D plus vinpocetine treated group. The left testis of each rat was subjected to unilateral torsion followed by detorsion after 2 h. Vinpocetine was administered intraperitoneally immediately and for 10 days following detorsion. At the end of the study, the rats were sacrificed and their testes removed and processed. HSP-70 expression, apoptosis and histopathological damage scores were determined for each group. Testicular T/D caused significant increases in apoptosis and HSP-70 expression, and a significant decrease in Johnsen's testicular biopsy scores and mean seminiferous tubule diameter. Vinpocetine ameliorated testicular histopathology and HSP-70 expression in the T/D + vinpocetine group. Consequently, vinpocetine may prevent testicular injury following testicular torsion owing to its antioxidant effects.

A biochemical and immunohistochemical study of the protective effects of carnosine for carbon tetrachloride induced liver injury in rats.

We investigated the protective effect of carnosine on carbon tetrachloride-induced liver tissue damage. Thirty-two adult male rats were divided into four equal groups. Group 1 was the untreated control, group 2 was injected with 0.2 ml/kg/day carbon tetrachloride, group 3 was injected with with 0.2 ml/kg/day carbon tetrachloride plus 200 mg/kg/day carnosine, and group 4 was injected with 200 mg/kg/day carnosine. Increased serum alanine amino transferase and aspartate amino transferase levels, liver malondialdehyde levels, HSP-70 expression and steatosis were observed following treatment with carbon tetrachloride. Carbon tetrachloride caused severe biochemical and histopathological changes in liver tissue and treatment with carnosine partially prevented the damage. HSP-70 may help control liver damage.

The effects of adriamycin on E-cadherin mediated cell-cell adhesion and apoptosis during early kidney development.

Adriamycin (ADR) is strongly teratogenic. We investigated the effects of ADR on apoptosis and the intensity of E-cadherin expression in developing kidneys. An experimental group of rats was given 2 mg/kg/day ADR on days 6-9 of gestation and a control group was given saline on the same schedule. Embryos were decapitated on days 13, 15, 17 and 19 of gestation, and processed and embedded in paraffin for routine light microscopy. Kidney specimens were stained with hematoxylin and eosin or periodic acid-Schiff, or immunostained for E-cadherin. Apoptosis was assessed using the TUNEL method. Weight loss and developmental deficiency were determined in embryos of the experimental group. ADR damaged or destroyed tubule epithelial cells, which caused apparent dilatation of the tubule lumen. Also, the brush borders of proximal tubules were damaged and glomerular spaces were dilated. ADR caused apoptosis of kidney tissue by days 15, 17 and 19 of development and E-cadherin expression was up-regulated during kidney development compared to controls. We found that ADR can cause apoptosis and increased E-cadherin expression in the developing rat kidney. E-cadherin expression and apoptosis may contribute to the development of ADR nephrotoxicity.

Intraperitoneal Administration of Low Dose Aluminium in The Rat: How Good is It to Produce a Model for Alzheimer Disease.

Since neurotoxicity of aluminium (Al) resembles the progressive neurodegeneration observed in Alzheimer Disease (AD), Al administration in several ways has been used to produce AD model. Intraperitoneal (ip) low dose (4.2 mg/ kg) Al injection in rats for long periods is the preferred method by some researchers. In this paper, the efficiency of this method for producing an AD model was evaluated. In this study, we looked at the neuropathology of Al and the characteristic lesions of AD by histological and immunohistochemical techniques and determined oxidative stress markers in the brains of Al-treated and control rats. We also made electrophysiological recordings at the hippocampus and evaluated possible behavioural changes by Morris water maze test. However, no pathologic changes occurred in the animals except for an impairment in long-term potentiation (LTP) in the hippocampus (e.g. the LTPs of population spike (PS) amplitude at 15 min post-tetanus were measured as 217±27% in Al-treated rats and as 240±42% in sham-treated rats, of baseline PS amplitude). According to the findings of the present study, low dose of ip Al in rats is not sufficient to produce a good AD model. Higher doses (≥10 mg/kg) should be used.

Intermediate filament protein nestin is expressed in developing meninges.

BACKGROUND: Nestin is a type VI intermediate filament protein known as a marker for progenitor cells that can be mostly found in tissues during the embryonic and fetal periods. In our study, we aimed to determine the expression of nestin in meninges covering the brain tissue at different developmental stages and in the new born. METHODS: In this study 10 human fetuses in different development stages between developmental weeks 9-34 and a newborn brain tissue were used. Fetuses in paraffin section were stained with H+E and nestin immunohistochemical staining protocol was performed. RESULTS: In this study, in the human meninges intense nestin expression was detected as early as in the 9th week of development. Intensity of this expression gradually decreased in later stages of development and nestin expression still persisted in a small population of newborn meningeal cells. CONCLUSION: In the present study, nestin positive cells gradually diminished in the developing and maturing meninges during the fetal period. This probably depends on initiation of a decrease in nestin expression and replacement with other tissue-specific intermediate filaments while the differentiation process continues. These differences can make significant contributions to the investigation and diagnosis of various pathological disorders (Tab. 1, Fig. 3, Ref. 36).

Antioxidant effect of carnosine treatment on renal oxidative stress in streptozotocin-induced diabetic rats.

Nitric oxide (NO) plays a significant role in the development of diabetic nephropathy. We investigated the effects of an antioxidant, carnosine, on streptozotocin (STZ)-induced renal injury in diabetic rats. We used four groups of eight rats: group 1, control; group 2, carnosine treated; group 3, untreated diabetic; group 4, carnosine treated diabetic. Kidneys were removed and processed, and sections were stained with periodic acid-Schiff (PAS) and subjected to eNOS immunohistochemistry. Examination by light microscopy revealed degenerated glomeruli, thickened basement membrane and glycogen accumulation in the tubules of diabetic kidneys. Carnosine treatment prevented the renal morphological damage caused by diabetes. Moreover, administration of carnosine decreased somewhat the oxidative damage of diabetic nephropathy. Appropriate doses of carnosine might be a useful therapeutic option to reduce oxidative stress and associated renal injury in diabetes mellitus.

Effect of melatonin and vitamin C on expression of endothelial NOS in heart of chronic alcoholic rats.

The aim of this study was to investigate the effects of melatonin and vitamin C on expression of endothelial nitric oxide synthase (NOS) in heart tissue of chronic alcoholic rats. Twenty-four adult male Wistar rats weighing 200-250 g were used in this study. Rats were divided into four groups. The first group served as control (n = 6). The second group was treated with ethanol (%7.2) for 28 days (n = 6), which was administered in artificial isocaloric diets. The third group was given ethanol and supplemented with 40 mg/kg vitamin C [intraperitoneally (i.p.)] (n = 6). The fourth group was given ethanol and supplemented with 4 mg/kg melatonin (i.p.) (n = 6). At the end of the experiment, rats were sacrificed and heart tissues were processed for immunohistochemistry analysis to endothelial NOS (eNOS). eNOS immunoreactivity showed heterogeneous distribution in control group. eNOS immunoreactivity was (+) in some myocytes and (++) in some others. Expression of eNOS in alcohol group was heterogeneous like control group but also stronger than that. Immunoreactivity was (+++) in myocytes near the epicardial zone and (++) in myocytes near the endocardium border. In melatonin and vitamin C-treated groups, eNOS immunoreactivity was diffuse and the intensity of reaction was (+++) in subepicardial region. However, eNOS immunoreactivity scores were weaker in these groups when compared with the alcohol group. Our results indicate that alleviation of oxidative stress by antioxidant therapy reduces reactive oxygen species-mediated nitric oxide inactivation.

Effects of melatonin and vitamin C on cigarette smoke-induced damage in the kidney.

This study was carried out to investigate smoke-induced structural and biochemical changes and protective effects of co-administered melatonin and vitamin C in the kidney. Twenty-four Wistar adult female rats were used in this study. Animals were divided into four groups. The first group rats were used as control. The second group of rats inhaled cigarette smoke. Smile smoke inhaling third and fourth group rats received melatonin and vitamin C, respectively. At the end of experimental study, kidney tissues and blood samples were taken under ether anesthesia. Tissues were prepared and examined by light microscopy. Malondialdehyde and glutathione levels and catalase activity were determined. By light microscopic observation, a decrease of Bowman space of some renal corpuscles, foamy-like tubules, dilatation and congestion of the peritubuler vessels, and atrophy of the some renal corpuscles were observed in group II. In groups III and IV melatonin and vitamin C relatively protected the kidney tissue against smoke intoxication. Biochemical examination showed that malondialdehyde and glutathione levels and catalase activity in group II were higher than in group I. Melatonin and vitamin C injection to group III and IV caused a decrease in malondialdehyde and glutathione levels. Catalase activity did not change in these groups. We have shown that cigarette smoke inhalation caused structural changes in the kidney. However, melatonin and vitamin C administration produced in some degree protection against smoke-induced damage.