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Biomedical subjects

Y Mao

Publications and source records attributed to Y Mao.

At least 235 records · Page 13Linked to original sources
PubMed1995

Inorganic components of drinking water and microalbuminuria.

Relatively little is known of the chronic effects attributable to the ingestion of inorganic components such as uranium and silicon. Although ingestion of large amounts of U can cause acute renal damage through a chemical effect, studies on humans have typically considered inhalation the route of exposure. We investigated the association between drinking water concentration levels of U and Si, and microalbuminuria, a sensitive biological indicator of renal dysfunction. Linear regression analysis revealed a statistically significant association between U cumulative exposure index and albumin per mmol creatinine (P = 0.03). No such significant relationship appeared for Si, although a positive trend was witnessed. Since normal but increasing levels of microalbuminuria were observed at U concentration levels below the Canadian Maximum Allowable Concentration (MAC), it is suggested that further study be undertaken.

Adolescent↗
PubMed1995

HPLC investigation on Ni(II)-mediated DNA damage in the presence of t-butyl hydroperoxide and glutathione.

By use of HPLC with UV and electrochemical detection, the present study demonstrates that reaction of Ni2+ with t-butyl hydroperoxide in the presence of glutathioine (GSH) generates 8-hydroxy-2'-deoxyguanosine (8-OH-dG) from 2'-deoxyguanosine (dG) and from dG residues in calf thymus DNA at physiological pH. No significant amount of 8-OH-dG was generated in the absence of GSH, indicating an important role of GSH in enhancing the reactivity of Ni2+ toward lipid hydroperoxide to oxidize dG or dG residues in DNA. The rate of dG conversion to 8-OH-dG depends on the concentration of the reagents. During a two hour incubation of 0.75 mM dG, 10 mM t-butyl hydroperoxide, 1 mM Ni2+, and 2 mM GSH at room temperature under ambient air, dG was converted to 8-OH-dG with a yield of about 0.2%. For dG residues in DNA, 24 hour incubation at 37 degrees C yielded 0.1% 8-OH-dG. The 8-OH-dG generation from both dG and dG residues in DNA was inhibited by superoxide dismutase, catalase, and ethanol (hydroxyl radical scavenger), implying the involvement of oxygen free radicals in the 8-OH-dG generation process. The metal ion chelators, deferoxamine and EDTA, efficiently inhibited the 8-OH-dG formation. Similar results were obtained for the conversion of dG residues in calf thymus DNA to 8-OH-dG. Electrophoretic assays of DNA strand breaks showed that Ni2+ caused DNA double-strand breaks in the presence of t-butyl hydroperoxide and GSH. Because GSH is ubiquitously present in cellular systems at relatively high concentration, and the exposure of cells to Ni2+ results in the generation of lipid hydroperoxides, the 8-OH-dG generation and DNA double-strand breaks caused by the reaction of Ni2+ with lipid hydroperoxides in the presence of GSH may be an important mechanism in Ni(2+)-induced carcinogenesis. The inhibitory effect of chelators suggests a possible prevention strategy against Ni(2+)-induced toxicity and carcinogenesis.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1995

Antioxidant activity of tetrandrine and its inhibition of quartz-induced lipid peroxidation.

Tetrandrine is a benzylisoquinoline alkaloid that has been used in China as an antifibrotic drug to treat the lesions of silicosis. Its mechanism in the treatment of silicosis is unclear. Electron spin resonance (ESR) spin trapping was employed to investigate the antioxidant properties of tetrandrine. The spin trap used was 5,5-dimethyl-1-pyrroline N-oxide (DMPO). Tetrandine efficiently reacted with hydroxyl (.OH) radicals with a reaction rate of approximately 1.4 x 10(10) M-1 s-1. The .OH radicals were generated by the Fenton reaction [Fe(II) + H2O2) as well as by reaction of chromium(V) with H2O2. Similar results were obtained using .OH radicals generated by reaction of freshly fractured quartz particles with aqueous medium. Tetrandrine also scavenged superoxide (O2-) radicals produced from xanthine/xanthine oxidase. The effect of tetrandrine on lipid peroxidation induced by freshly fractured quartz particles was evaluated using linoleic acid as a model lipid. The results showed that tetrandrine caused a significant inhibition on freshly fractured quartz-induced lipid peroxidation.

Alkaloids↗
PubMed1995

Chromium(VI)-induced nuclear factor-kappa B activation in intact cells via free radical reactions.

Incubation of chromium(VI) [Cr(VI)] with cultured Jurkat cells resulted in activation of DNA binding activity of the nuclear factor (NF)-kappa B. In a combination with glutathione reductase, a Cr(VI) reducing agent, Cr(VI) expressed an enhanced activity in induction of NF-kappa B. This activation of NF-kappa B was decreased by a metal chelator, diethylene-triaminepentaacetic acid or catalase, but increased by superoxide dismutase. Addition of Mn2+, which reacts with Cr(IV) and inhibits Cr(IV)-mediated hydroxyl radical (.OH) generation via Fenton-like reaction, attenuated the activation of NF-kappa B. Sodium formate, an .OH radical scavenger, also inhibited the activation. Electron spin resonance measurements showed that the incubation of Cr(VI) with intact Jurkat cells generated reactive Cr(V) intermediate. Glutathione reductase and NADPH enhanced Cr(V) generation. Electron spin resonance spin trapping measurements using 5,5-dimethyl-1-pyrroline N-oxide (DMPO) as a spin trapping agent provided evidence that the incubation of Cr(VI) with the Jurkat cells in the presence of glutathione reductase generated .OH radicals. H2O2 enhanced .OH radical generation and also enhanced Cr(V) formation, indicating the role of Cr(IV) in .OH radical generation. We conclude that Cr(VI) can activate NF-kappa B in vitro via Cr(IV)-mediated free radical reactions. We hypothesize that Cr(VI)-mediated NF-kappa B activation may be involved in the mechanism of Cr(VI)-induced carcinogenicity.

Base Sequence↗
PubMed1995

Extracting direction and curvature features of jaw movement traces with chain code.

Frontal chewing patterns have been classified in a manual and visual way on recorded movement tracks. The main aim of this study was to use a chain code method to extract the direction and curvature features of the tracks in the frontal plane. The test results indicate that the chain code can stand for the direction and curvature. The chewing movement tracks in the frontal plane can be clustered into chain code values. The method therefore appears to be useful in the classification of chewing movements.

Humans↗
PubMed1995

[The relationship between preoperative small airway function tests and postoperative airway infection in patients with esophageal carcinoma].

The article reports the results of preoperative small airway function tests among 116 cases of esophageal carcinoma and its relationship with the postoperative airway infection. Among three main parameters reflecting narrowing of small airway, %V25/HT is the most sensitive one, %MMEF comes next, and %FEV1 the least, Eight-eight of 116 cases without any other postoperative complications were enrolled. The morbidity of postoperative airway infection in this group was 62.5%. They were divided into three groups according to %V25/HT: group I with normal small airway function (%V25/HT > 70%, 26 cases), group II with moderately deviated function (%V25/HT 46-70%, 31 cases), group III with severely deviated function (%V25/HT < 45%, 31 cases). The morbidity rate of postoperative airway infection and the average fever period in the three groups were 50%, 51.6%, 83.3% and 60, 74, 108 hours, respectively. The difference between group I and group III, between group II and group III are significant statistically both in the morbidity rate and the fever period of postoperative airway infection. If divided by different modes of operation, the average postoperative fever perioed in intrathoracic and neck anastomosis group was 79 and 105 hours. The difference between the above two groups is remarkable but not significant statistically. The results come to a conclusion that the patients undergoing larger operation and with more severe abnormal small airway function usually have longer and more severe postoperative airway infection.

Adult↗
PubMed1995

Singlet oxygen generation in the superoxide reaction.

ESR spin trapping was utilized to study the singlet oxygen (1O2) generation in the reaction of superoxide (O2) with H2O2. The spin trap used was 2,2,6,6-tetramethyl-4-piperdone. Incubation of xanthine, xanthine oxidase and H2O2 generated 1O2 spin adduct signal. Omission of xanthine, xanthine oxidase or H2O2 caused a sharp decrease in 1O2 generation. 1O2 scavenger, sodium azide, inhibited 1O2 generation while .OH scavenger, ethanol, only slightly decreased the signal intensity. Potassium superoxide (KO2) decomposition generated 1O2. Catalase and sodium azide inhibited 1O2 generation and H2O2 enhanced it. The results demonstrate that O2 is capable of generating 1O2 upon reaction with H2O2.

Azides↗
PubMed1995

Generation of free radicals by Cr(IV) from lipid hydroperoxides and its inhibition by chelators.

The generation of free radicals by Cr(IV) from lipid hydroperoxides was investigated by ESR spin trapping. The spin trap used was 5,5-dimethyl-1-pyrroline N-oxide (DMPO). Reaction of Cr(VI) with ascorbate was used as a source of Cr(IV). Incubation of Cr(VI) with ascorbate generated Cr(IV) and Cr(V). Addition of cumene hydroperoxide generated DMPO/R adduct with an enhancement of Cr(V) signal. Addition of Mn(II), whose function is to remove Cr(IV), caused dose-dependent inhibition of DMPO/R formation. Similar results were obtained using t-butyl hydroperoxide. Metal ion chelators, deferoxamine, 1,10-phenanthroline and diethylenetriaminepentaacetic acid inhibited DMPO/R formation in the order of deferoxamine > 1,10-phenanthroline > diethylenetriaminepentaacetic acid. The results suggest the possible role of Cr(IV) and its mediated free radical generation from lipid hydroperoxides in the mechanism of Cr(VI) carcinogenesis.

Ascorbic Acid↗
PubMed1995

[Molecular diagnosis of Huntington's disease: an analysis of two large families].

At present molecular techniques comprise a main resource in the early accurate diagnosis for Huntington's disease. We describe the molecular diagnosis for 8 HD patients and 39 risky family members in two large HD pedigrees by using G8 RFLP linkage analysis as well as direct detection of the expanded (CAG) repeat in IT15 gene with the nested PCR denaturing polyacrylamide gel electrophoretic autoradiography and direct DNA sequencing. The results showed that the normal IT15 alleles contained 13 to 26 CAG repeat but major in 16, while all the HD alleles had over 40 copies of (CAG)n. There was no overlap between the normal and affected alleles. The presymptomatic diagnosis of 39 family members at risk for HD disclosed that 11 subjects carried the affected alleles. All these results indicated that the unstable mutations in IT15 gene were responsible for HD in the Chinese. They also provide valuable data for HD molecular diagnosis, genetic counselling and genetic health.

Adolescent↗
PubMed1995

Direct interaction between crystalline silica and DNA - a proposed model for silica carcinogenesis.

Crystalline silica in aqueous buffer produced oxygen radicals that mediated in vitro DNA (deoxyribonucleic acid) strand breakage. The oxidized DNA base, thymine glycol, was also produced. The hydroxyl radical, responsible for most DNA damage, has a reaction distance of about 15 Angstroms, requiring close contact of silica with DNA. Fourier transform infrared spectroscopy of incubations of quartz particles with DNA showed distinct alterations in both DNA and quartz spectra and therefore indicated extensive hydrogen bonding between surface silanol groups and the phosphate-sugar backbone of DNA. Electron microscopy and energy dispersive X-ray spectroscopy of alveolar epithelial cells in fetal rat lung, exposed to quartz in culture, showed localization of quartz particles in the nuclei and mitotic spindles. Direct interaction of crystalline silica with DNA may be important in silica carcinogenesis by anchoring DNA close to sites of free radical production on the silica surface, or by interfering with DNA replication, repair, or the mitotic process.

Animals↗
PubMed1994

8-Hydroxy-2'-deoxyguanosine formation and DNA damage induced by sulfur trioxide anion radicals.

The 8-hydroxy-2'-deoxyguanosine (8-OHdG) formation and DNA damage by sulfur trioxide anion radicals (SO3.-) were investigated using ESR spin trapping, HPLC, and electrophoretic assays. Sulfite (SO3(2-) autoxidation generated both hydroxyl (.OH) and SO3.- radicals. Oxidation of SO3(2-) by chromium (VI) generated only SO3.- with much enhanced yield. Incubation of 2'-deoxyguanosine (dG) with SO3(2-) generated 8-OHdG albeit at low yield. Chromium (VI) enhanced the yield four-fold. Electrophoretic assays showed that SO3.- radicals generated by chromium (VI) oxidation of SO3(2-) caused DNA double strand breaks. The results demonstrate that SO3.- radicals are capable of causing dG hydroxylation and DNA double strand breaks.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1994

Generation of thiyl and ascorbyl radicals in the reaction of peroxynitrite with thiols and ascorbate at physiological pH.

Electron spin resonance (ESR) spin trapping was utilized to investigate the reaction of peroxynitrite with thiols and ascorbate at physiological pH. The spin trap used was 5,5-dimethyl-1-pyrroline N-oxide (DMPO). The reaction of peroxynitrite with DMPO generated 5,5-dimethylpyrrolidone-(2)-oxy-(1) (DMPOX). Formate enhanced the peroxynitrite decomposition but did not generate any detectable amount of formate-derived free radicals. Thus, the spin trapping measurements provided no evidence for hydroxyl (.OH) radical generation in peroxynitrite decomposition at physiological pH. Thiols (glutathione, cysteine, and penicillamine) and ascorbate reacted with peroxynitrite to generate the corresponding thiyl and ascorbyl radicals. The one-electron oxidation of thiols by peroxynitrite may be one of the important mechanisms for peroxynitrite-induced toxicity and ascorbate may provide a detoxification pathway.

Ascorbic Acid↗
PubMed1994

ESR spin trapping investigation on peroxynitrite decomposition: no evidence for hydroxyl radical production.

The decomposition of peroxynitrite in the presence of 5,5-dimethyl-1-pyrroline N-oxide (DMPO) generated 5,5-dimethylpyrrolidone-(2)-oxy-(1) (DMPOX) without formation of DMPO/OH. Formate enhanced the peroxynitrite decomposition but did not generate any detectable amount of formate-derived free radicals. Glutathione, cysteine, penicillamine, and ascorbate reacted with peroxynitrite to generate the corresponding thiyl and ascorbyl radicals. The results show that the decomposition of peroxynitrite did not generate any significant amount of OH radicals, and one-electron reduction of peroxynitrite by ascorbate may be one of the important peroxynitrite detoxification pathways.

Ascorbic Acid↗
PubMed1994

Reaction of Cr(VI) with ascorbate and hydrogen peroxide generates hydroxyl radicals and causes DNA damage: role of a Cr(IV)-mediated Fenton-like reaction.

Incubation of Cr(VI) with ascorbate generated Cr(V), Cr(IV) and ascorbate-derived carbon-centered alkyl radicals, as well as formyl radicals. H2O2 caused generation of hydroxyl radicals (OH) and much higher levels of Cr(V), showing that .OH can be generated via a Cr(IV)-mediated Fenton-like reaction (Cr(IV) + H2O2-->Cr(V) + .OH + OH-). 1,10-Phenanthroline and deferoxamine inhibited the formation of both .OH and Cr(V) from the reaction of Cr(VI) with ascorbate in the presence of H2O2. Electrophoretic assays showed that ascorbate-derived free radicals caused DNA double-strand breaks. .OH radicals generated by Cr(V)- and Cr(IV)-mediated Fenton-like reactions also caused DNA double-strand breaks. HPLC measurements showed that .OH radicals generated by Cr(IV) and Cr(V) from H2O2 caused 2'-deoxyguanine hydroxylation to form 8-hydroxy-2'-deoxyguanine.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1994

Serum iron and risk of fatal acute myocardial infarction.

We assessed the relation of serum iron, dietary iron, and the use of iron supplements to the risk of fatal acute myocardial infarction in the Nutrition Canada Survey cohort. We found an association between serum iron and risk of fatal acute myocardial infarction, with rate ratios for males and females in the highest category of serum iron (> or = 175 micrograms per dl) of 2.18 [95% confidence intervals (CI) = 1.01-4.74] and 5.53 (95% CI = 1.69-18.12), respectively. We found no important association between risk of fatal acute myocardial infarction and either dietary iron or iron supplement use among the 9,920 participants included in this study.

Acute Disease↗
PubMed1994

Correlation between autoregressive moving-average model parameters of electromyogram of human jaw closing muscles and maximum clenching time at intercuspal position.

During maximum clenching in the intercuspal position, surface electromyograms of left masseter and anterior temporal muscles were sampled in 16 healthy subjects with natural dentitions to establish a four-order, autoregressive (AR) moving-average (MA) model of the myoelectrical signals. The correlation coefficients and the linear regression between the model parameters and the clenching time were calculated. The model parameters had the positive or the negative correlation, and AR model parameters had the higher correlation than MA model parameters. The model parameters relate to muscular fatigue and the slope of the regressive equation relates to the endurance time of the isometric contraction.

Adult↗
PubMed1994

Silica radical-induced DNA damage and lipid peroxidation.

In recent years, more attention has been given to the mechanism of disease induction caused by the surface properties of minerals. In this respect, specific research needs to be focused on the biologic interactions of oxygen radicals generated by mineral particles resulting in cell injury and DNA damage leading to fibrogenesis and carcinogenesis. In this investigation, we used electron spin resonance (ESR) and spin trapping to study oxygen radical generation from aqueous suspensions of freshly fractured crystalline silica. Hydroxyl radical (.OH), superoxide radical (O2.-) and singlet oxygen (1O2) were all detected. Superoxide dismutase (SOD) partially inhibited .OH yield, whereas catalase abolished .OH generation. H2O2 enhanced .OH generation while deferoxamine inhibited it, indicating that .OH is generated via a Haber-Weiss type reaction. These spin trapping measurements provide the first evidence that aqueous suspensions of silica particles generate O2.- and 1O2. Oxygen consumption measurements indicate that freshly fractured silica uses molecular oxygen to generate O2.- and 1O2. Electrophoretic assays of in vitro DNA strand breakages showed that freshly fractured silica induced DNA strand breakage, which was inhibited by catalase and enhanced by H2O2. In an argon atmosphere, DNA damage was suppressed, showing that molecular oxygen is required for the silica-induced DNA damage. Incubation of freshly fractured silica with linoleic acid generated linoleic acid-derived free radicals and caused dose-dependent lipid peroxidation as measured by ESR spin trapping and malondialdehyde formation. SOD, catalase, and sodium benzoate inhibited lipid peroxidation by 49, 52, and 75%, respectively, again showing the role of oxygen radicals in silica-induced lipid peroxidation.(ABSTRACT TRUNCATED AT 250 WORDS)

DNA Damage↗