The effect of p,p'-DDT (dicophane) and its main metabolites on the respiration of rat liver mitochondria

The effects of DDT, DDE, DDOH and DDA on the oxidation of NADH, glutamate, -hydroxybutyrate and sucoinate by rat liver mitochondria were investigated. The influence of these compounds on the activity of purified liver glutamate dehydrogenase was also checked. It was found that DDT and all those of its metabolites investigated inhibited oxidation of NAD-linked substrates by both intact and sonicated mitochondria. The water-soluble metabolites of DDT (DDOH and DDA) stimulated succinate oxidation by intact but not by sonicated mitochondria, and inhibited the activity of glutamate dehydrogenase. It is concluded that DDT and its metabolites may affect mitochondrial respiratory chain between NADH and CoQ, inhibit glutamate dehydrogenase, and uncouple oxidative phosphorylation.     

Lactate dehydrogenase isoenzymes in tumours of the nervous system

Summary The variations in the isoenzymes of lactic acid dehydrogenase have been studied in a series of tumours of the nervous system. From these the ratio of heart muscle component to skeletal muscle component (the H/M ratio) has been calculated and compared with the H/M ratio of a variety of regions of normal brain. Oligodendrogliomata were found to have a very high H/M ratio. There was a decrease in the ratio with increasing degrees of de-differentiation of all tumours studied. However the H/M ratio does not appear directly related to the rate of growth irrespective of the tissue of origin of the tumour. Tumours derived from different tissues appear to have their own range of ratios. Tumour cyst fluids showed similar ratios to their parent tumours.     

解酒保肝口服液对小鼠酒精中毒的影响

目的：观察解酒保肝口服液对小鼠醉酒实验,血清乙醇浓度和肝、胃组织乙醇脱氢酶活性的影响。方法：将生理盐水和将葛根,甘草等中药用水煎煮制成解酒保肝口服液灌服于小鼠后30min,灌服白酒,记录小鼠翻正反射消失（醉酒）至恢复（醒酒）所需时间（min),及24h内小鼠的死亡只数,另以相同操作连续6d后眼眶取血并处死动物,立即取出肝脏和胃,分别用生化比色法测定血肖乙醇浓度和肝、胃组织乙醇脱氢酶活性。结果：在醉酒实验中,。与对照组相比服用解酒保肝口服液组小鼠从饮酒到翻正反射消失（醉酒）的时间明显延长（P＜0．01）,醒酒时间明显缩短,且小鼠的死亡率明显降低（P＜0．05）,血清乙醇含量明显降低,肝脏ADH高于对照组, 结论：解酒保肝口服液具有解酒作用。     

Quantitative Elisa for Human Lactate Dehydrogenase Isoenzyme 5

Abstract

Four monoclonal antibodies (Mab) derived from mice immunized with lactate dehydrogenase 5 (LDH5) react strongly with LDH5, but weakly with LDH2 which contains a single subunit of type M. Experimental evidence suggests that these antibodies are directed to an antigenic determinant in the interface between two subunits of type M. A sandwich ELISA procedure was devised, using these Mabs to identify and quantify LDH5. The procedure involves immobilization of one of these Mabs by its adsorption onto polyclonal anti-mouse IgG coated polystyrene plates, adsorption of LDH5, its identification by the same Mab as that used in the immobilization step, and finally color development by an enzyme labeled rabbit anti-mouse IgG antiserum. The method enables LDH5 to be assayed at a concentration range of 0–5 μg/ml.     

纳米细菌对人脐静脉内皮细胞的损伤及超氧化物歧化酶分泌的影响

目的探讨纳米细菌对人脐静脉内皮细胞(HUVEC)的损伤及超氧化物歧化酶(SOD)分泌的影响。方法用含有不同浓度纳米细菌的培养液培养HUVEC,采用四甲基偶氮唑盐法检测细胞活力;用浓度为0.5 Mcfarland纳米细菌攻击HUVEC,分别于0、6、12、24、48、72 h检测培养液上清中乳酸脱氢酶(LDH)、丙二醛(MDA)和SOD水平。结果与对照组比较,纳米细菌(吸光度值为0.001、0.005和0.02)处理HUVEC CRL2480细胞48、72 h后,细胞活力显著降低(P0.05);与对照组比较,纳米细菌处理组细胞培养液中LDH和SOD浓度显著增高(P0.05),而MDA含量无显著变化(P0.05)。结论纳米细菌能损伤HUVEC,同时增加HUVEC中SOD活性。     

Genetic Polymorphism of Cytochrome P-4502E1 and Mitochondrial Aldehyde Dehydrogenase in a Korean Population

Mitochondrial aldehyde dehydrogenase (ALDH2) is mainly responsible for the oxidation of acetaldehyde generated during alcohol oxidation in vivo. Cytochrome P-4502E1 (CYP2E1), a liver microsomal enzyme, also metabolizes acetaldehyde and ethanol. Genetic polymorphism of ALDH2 and CYP2E1 was investigated among 481 Korean adults. A new restriction fragment-length polymorphism method was developed to determine the genotype of the ALDH2 alleles. This method proved to be simpler and faster than the hybridization method using allele-specific oligonucleotide probes and polymerase chain reaction-directed mutagenesis. The allele frequencies of ALDH2¹ and ALDH2² were 0.840 and 0.160, respectively. This allele frequency of ALDH2² is less than in Japanese people. Genetic polymorphism of CYP2E1 was investigated using polymerase chain reaction and restriction fragment-length polymorphism. The estimated allele frequencies for C1 and c2 were 0.808 and 0.192.     

Acetaldehyde production and other ADH-related characteristics of aerobic bacteria isolated from hypochlorhydric human stomach

BACKGROUND: Acetaldehyde is a known local carcinogen in the digestive tract in humans. Bacterial overgrowth in the hypochlorhydric stomach enhances production of acetaldehyde from ethanol in vivo after alcohol ingestion. Therefore, microbially produced acetaldehyde may be a potential risk factor for alcohol-related gastric and cardiac cancers. This study was aimed to investigate which bacterial species and/or groups are responsible for acetaldehyde formation in the hypochlorhydric human stomach and to characterize their alcohol dehydrogenase (ADH) enzymes. METHODS: After 7 days of treatment with 30 mg of lansoprazole twice a day, a gastroscopy was performed on eight volunteers to obtain hypochlorhydric gastric juice. Samples were cultured and bacteria were isolated and identified; thereafter, their acetaldehyde production capacity was measured gas chromatographically by incubating intact bacterial suspensions with ethanol at 37 degrees C. Cytosolic ADH activities, Km values, and protein concentration were determined spectrophotometrically. RESULTS: Acetaldehyde production of the isolated bacterial strains (n = 51) varied from less than 1 to 13,690 nmol of acetaldehyde/10(9) colony-forming units/hr. ADH activity of the strains that produced more than 100 nmol of acetaldehyde/10(9) colony-forming units/hr (n = 23) varied from 3.9 to 1253 nmol of nicotinamide adenine dinucleotide per minute per milligram of protein, and Km values for ethanol ranged from 0.65 to 116 mM and from 0.5 to 3.1 M (high Km). There was a statistically significant correlation (r = 0.64, p < 0.001) between ADH activity and acetaldehyde production from ethanol in the tested strains. The most potent acetaldehyde producers were Neisseria and Rothia species and Streptococcus salivarius, whereas nearly all Stomatococcus, Staphylococcus, and other Streptococcus species had a very low capacity to produce acetaldehyde. CONCLUSIONS: This study demonstrated that certain bacterial species or groups that originate from the oral cavity are responsible for the bulk of acetaldehyde production in the hypochlorhydric stomach. These findings provide new information with the respect to the local production of carcinogenic acetaldehyde in the upper digestive tract of achlorhydric human subjects.     

Differential Expression of Mitochondria1 NADH Dehydrogenase in Ethanol-Treated Rat Brain: Revealed by Differential Display

The technique of polymerase chain reaction (PCR) differential display was used to detect alterations in gene expression after chronic alcohol administration. Male Wistar rats were treated with ethanol vapor for 14 days. The cDNA generated from mRNA isolated from the hippocampi of ethanol-treated and control animals was compared by PCR differential display. A differentially expressed cDNA fragment was used to screen mRNA samples by Northern analysis. The level of a mRNA was significantly elevated (× 2.5) in the hippocampus, but not the cortex of alcohol-treated rats up to 48 hr after withdrawal. Sequence analysis of the cDNA fragment revealed an almost perfect homology to rat mitochondrial NADH dehydrogenase subunit 4 mRNA. The selective induction of this mRNA in alcohol-treated rat brain areas suggests altered metabolic processes and possible dysfunction of the mitochondria. The technique of PCR differential display may prove useful in further analysis of gene expression during alcohol dependence and withdrawal.