How defective spermatogenesis affects sperm DNA integrity

Spermatogenesis is the essential process to maintain and promote male fertility. It is extraordinarily complex with many regulatory elements and numerous steps. The process involves several cell types, regulatory molecules, repair mechanisms and epigenetic regulators. Evidence has shown that fertility can be negatively impacted by reduced sperm DNA integrity. Sources of sperm DNA damage include replication errors and causes of DNA fragmentation which include abortive apoptosis, defective maturation and oxidative stress. This review outlines the process of spermatogenesis, spermatogonial regulation and sperm differentiation; additionally, DNA damage and currently studied DNA repair mechanisms in spermatozoon are also covered.     

丹皮酚对增生性瘢痕成纤维细胞的抑制作用

目的探讨丹皮酚对增生性瘢痕成纤维细胞的抑制作用。方法自2018年9月至2020年6月北部战区总医院烧伤整形科提取原代增生性瘢痕成纤维细胞后,将细胞平分为4组,分别采用0μmol/L(对照组)、50μmol/L、100μmol/L的丹皮酚及10μmol/L的5-氟尿嘧啶(5-Fu)处理;CCK-8实验检测细胞处理后第0、3、5、7天的增殖情况。处理3 d后通过ELISA实验检测增生性成纤维细胞中活性氧基团或分子、丙二醛和超氧化物歧化酶的含量;Western blot实验检测丹皮酚对于细胞中TGF-β1、Ⅰ和Ⅲ型胶原的表达情况。结果50、100μmol/L的丹皮酚和10μmol/L的5-FU分别作用于细胞3 d后与对照组相比,对于细胞增殖的抑制率分别为(32.63±3.06)%、(46.41±4.41)%和(45.32±9.26)%,组间比较差异显著,具有统计学意义(P<0.05)。丹皮酚能够显著下调增生性成纤维细胞中ROS和MDA的表达情况,上调SOD的含量,降低TGF-β1、Ⅰ和Ⅲ型胶原的表达。结论丹皮酚能够抑制增生性瘢痕成纤维细胞的生长、减轻氧化应激损伤,下调TGF-β1和胶原的表达。     

The impact of DNA damage, genetic mutation and cellular responses on cancer prevention, longevity and aging: observations in humans and mice

Over the past 5 years, data collected from the mouse suggest that pathways important for either preventing or resolving DNA damage are longevity assurance mechanisms whose critical overall function is somatic cell maintenance, a necessary part of cancer prevention. These pathways include those that reduce DNA damage levels caused by exogenous sources, replication errors and by-products of cellular respiration. Unresolved DNA damage leads to permanent mutations in the genetic code that may be oncogenic. Therefore, pathways that resolve DNA damage are important anti-cancer mechanisms. As an important line of defense, there are a variety of pathways that repair DNA damage. In addition, there are anti-cancer pathways that respond to DNA damage by either preventing cellular replication or inducing cell death. Genes in these pathways, termed longevity assurance genes (LAG), code for proteins that reduce cancer incidence and as a result assures a sufficiently long health span needed for reproduction. Data from mouse models, many that were originally designed to study cancer, are showing that a potential consequence of DNA damage and responses to DNA damage is aging; these models support the hypothesis that at least some aspects of normal aging are the consequence of anticancer mechanisms designed to deal with damaged DNA.     

硒对大鼠肝细胞DNA损伤的体内体外研究

应用单细胞凝胶电泳研究了一定剂量的亚硒酸钠对离体和在体大鼠肝细胞 DNA损伤的作用。结果表明 :在2 .185、 4.375、 8.75 0、 17.5 0 0、 35 .0 0 0 μmol/ L 的剂量条件下 ,除 2 .185 μmol/ L 的剂量外 ,其余剂量的亚硒酸钠均可引起离体大鼠肝细胞 DNA损伤。 5、 10、 2 0 μmol/ kg的亚硒酸钠也可引起在体大鼠肝细胞 DNA损伤。亚硒酸钠引起的离体和在体大鼠肝细胞 DNA损伤均存在明显的剂量 -反应关系。研究结果提示 ,一定剂量的亚硒酸钠能引起离体和在体大鼠肝细胞 DNA损伤     

各种肝病患者血清TGFα含量与肝细胞损害的关系研究

目的 :探讨转化生长因子α(Transforminggrowthfactor aplha ,TGFα)在各种肝病患者中的变化规律及其与肝细胞损害的关系。方法 :采用非平衡竞争性放射免疫法测定 172例各种肝病患者血清中TGFα含量。结果 :慢性中度肝炎、急性黄疸肝炎、慢性重度肝炎、肝硬化失代偿期、原发性肝癌患者血清TGFα含量分别为 12 .12± 7.35pg ml、14.19± 7.30 pg ml、15 74±9 6 5pg ml、16 .0 2± 9.18pg ml、19.89± 9.0 9pg ml,逐渐升高 ,明显高于对照组 6 .86± 0 .89pg ml(P <0 .0 5)。肝硬化失代偿期与代偿期组间差异有显著性 (P <0 .0 5)。结论 :血清TGFα含量明显升高对原发性肝癌的诊断有帮助。TGFα与各种肝病肝细胞的再生、分化、增殖以及损害有一定的关系。     

32例恙虫病患者肾损害临床分析

目的：探讨恙虫病肾损害的临床特点。方法：从收治的１２８例恙虫病中选取有肾损害的３２例进行临床分析。结果：本组病例除具有恙虫病特征性的临床表现外,均有浮肿、尿少、尿蛋白、尿中红细胞,血压升高,ＵＮ及Ｃｒ升高等肾损害表现,发生率为４０％,使用特效抗菌药物及保肾治疗后,疗效满意。结论：加强对恙虫病肾损害的认识,可减少误诊误治。     

Benzodiazepine binding sites in alcoholic cirrhotics: evidence for gender differences

Synaptic plasma membranes were prepared from superior frontal gyrus and motor cortex obtained at autopsy from 17 chronic alcoholics not differentiated on thiamine status, of whom 8 had pathologically confirmed cirrhosis of the liver, and 10 controls. Three of the cirrhotic alcoholic cases were female, as was one control. Cases were closely matched for age at death and post-mortem delay. The affinity of central-type benzodiazepine sites for [³H]diazepam tended to be lower in both brain regions of both groups of alcoholics ofcf controls, but the reverse was true for [³H]flunitrazepam, especially in cirrhotic cases. [³H]Diazepam affinity was invariant across all males and the female control, but lower in the female cirrhotic alcoholics. Affinity for [³H]flunitrazepam tended to be the reverse of that for [³H]diazepam. [³H]Diazepam B_max was markedly lower in female cirrhotic alcoholics, especially in superior frontal gyrus, whereas this region showed a much higher B_max in the female control case. A small regional difference in [³H]flunitrazepam B_max was the reverse of that for [³H]diazepam B_max and was seen in all groups. GABA-mediated neurotransmission may be selectively altered in a pathologically abnormal region of cerebral cortex in cirrhotic alcoholics, and the sexes may show differing susceptibilities to change.     

铬结合物在铬中毒性肝损害中的作用

目的了解各种铬结合物与肝损害的关系。方法在铬中毒性肝损害的大鼠模型中,采用ＳｅｐｈａｄｅｘＧ５０凝胶层析技术,对肝中铬结合物进行分离和测定。结果铬染毒大鼠肝组织中,除可检出高分子铬结合物（ＨＭＷＣｒ,相对分子质量（ＭＷ）７００００～１２５００）及低分子铬结合物（ＬＭＷＣｒ,ＭＷ１２５００～５００）外,还发现对照组未检出的小分子铬结合物（ＭＭＷＣｒ,ＭＷ＜５００）。随染毒时间延长,肝损害加重,三者肝中分布变化明显：ＨＭＷＣｒ由２２．２％增至３７．０％;ＭＭＷＣｒ由２．２％增至５．０％;ＬＭＷＣｒ则从７５．６％降至５８．０％。结论ＬＭＷＣｒ可能与铬的解毒有关;ＭＭＷＣｒ的出现并增多反映了机体形成ＬＭＷＣｒ能力的紧张;ＭＭＷＣｒ可能是攻击靶器官的主要活性因素。     

高晶体-高胶体渗透压溶液对受机械性损伤的海马神经细胞容积的影响

观察机械性损伤的海马神经细胞在不同浓度高晶体－ 高胶体渗透压溶液中容积的变化。取原代培养大白鼠胚胎的海马神经细胞,用超声波机械损伤细胞后暴露于含０．５ ｇ／Ｌ、１ ｇ／Ｌ和２．５ ｇ／Ｌ氯化钠的细胞培养基中１５ ｍ ｉｎ。结果显示机械性损伤的细胞明显肿胀（Ｐ＜ ０．０５）。当细胞暴露于不同浓度的高晶体－ 高胶体溶液１５ ｍ ｉｎ 后, 细胞容积与同一实验时间的对照值相比明显下降, 并保持至第７ ｄ （Ｐ＜ ０．０５）。表明受到机械性损伤的海马神经细胞在高晶体－ 高胶体渗透压环境中的容积调节功能丧失或减弱。