The Effects of Vasectomy on Testicular Tissue of Mice: Histological Changes and DNA Fragmentation Study

Introduction: We aim to investigate the effect of vasectomy on the histology of the testis as well as to evaluate DNA fragmentation in testicular tissue of male mice. Methods: Bilateral vasectomy was performed on 20 mature male mice; 10 control mice underwent sham-operation. After 6 weeks, the testes were evaluated for histological changes and DNA fragmentation by single cell gel electrophoresis (comet assay). Results: Marked alterations were observed in the testes of vasectomized mice, including degeneration of spermatids, thickened basement membrane, dilatation of the seminiferous tubules, exfoliation of germ cells, reduction in the seminiferous cell population, vacuolated appearance of the epithelium in the tubules and marked interstitial fibrosis. Single cell gel electrophoresis showed a highly significant (P<0.0001) increase in DNA damage among vasectomized mice (46.02%) compared with control group (%27.17) after six weeks of operation. Conclusion: Vasectomy induced deterioration in the seminiferous tubules associated with increased testicular cell’s DNA fragmentation.

Preparation of β-CD–Quercetin Complex and its Effects on Ethanol- Damaged BRL-3A Hepatocytes

Objective: To prepare the sustained-release complex, quercetin was incorporated with β- cyclodextrin (β-CD) and the effect of β-CD–quercetin complex on the growth of ethanol-injuried hepatocytes was studied. Methods: By using scanning electron microscopy, infrared spectroscopy, and release rate analysis, β- CD–quercetin complex was identified. The effect of different concentrations of β-CD–quercetin complex on the growth of ethanol-damaged hepatocytes at different time was observed by using MTT assay, and the cell quantity and morphology were observed by using hematoxylin–eosin staining. By using single-cell gel electrophoresis, the prevention of β-CD–quercetin complex from the DNA damage of ethanol-damaged BRL-3A cells was studied, and Olive tail moment was calculated. Results: β-CD–quercetin complex as the sustained-release complex was successfully prepared. The ethanol induced damage of BRL-3A cells could be prevented by 20, 40 and 80 mg/L of quercetin complex, and the protection mechanism of hepatocyte was related to the antioxidation of DNA. Conclusion: Quercetin sustained-release complex could be prepared with β-CD, and it might be used to treat alcoholic liver disease.

The effect of different tobacco tar levels on DNA damage in cigarette smoking subjects

Objective To explore the genetic damage caused by different tar levels in the human body. Methods The subjects were divided into high, medium and low (12 mg, 8 mg, 5 mg) tar groups according to the tar levels. Nonsmoking populations served as a control group. 2 ml of peripheral blood was collected on the 10th day after morning fasting. Oxidative and genetic toxicological damage indicators were analysed with enzyme-linked immunosorbent assay, cytokinesis-block micronucleus assay in human lymphocyte and single cell gel electrophoresis. Results The distribution of hOGG1 concentration was significantly different within all groups, P &lt; 0.01. The concentrations of cotinine, 8-OHdG and Rap-2b were significantly differences between control and medium tar group, control and high tar group, low and medium tar group and low and high tar group, respectively, P &lt; 0.05. The level of PAH-DNA adducts was not significantly changed in the middle tar group and high tar group, P &gt; 0.05. The level of CRP was significantly changed between control and high tar group, low and high tar group and medium and high tar group, respectively, P &lt; 0.0001. The rate of comet tailing was significantly different between all groups. The rate of micronucleus cells was not significantly different between all groups. Conclusions The increase of tar content could increase the DNA damage to a certain extent, so the intake of tar content should be monitored.