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Biomedical subjects

Y Mao

Publications and source records attributed to Y Mao.

329 records · Page 19Linked to original sources

Vanadium(IV) causes 2'-deoxyguanosine hydroxylation and deoxyribonucleic acid damage via free radical reactions.

Vanadium(IV) caused molecular oxygen dependent 2'-deoxyguanosine (dG) hydroxylation to form 8-hydroxyl-2'-deoxyguanosine (8-OHdG). During a 15-minute incubation of 1.0 mM dG and 1.0 mM VOSO4 (vanadium(IV)) in phosphate buffer solution (pH 7.4) at room temperature under ambient air, dG was converted to 8-OHdG with a yield of about 0.31 percent. Catalase and formate inhibited the 8-OHdG formation while superoxide dismutase enhanced it. Diethylenetriaminepentaacetic acid (DTPA) and deferoxamine blocked the 8-OHdG formation. Incubation of vanadium(IV) with dG in argon did not generate any significant amount of 8-OHdG, indicating the role of molecular oxygen in the mechanism of vanadium(IV)-induced dG hydroxylation. Vanadium(IV) also caused molecular oxygen dependent deoxyribonucleic acid (DNA) strand breaks in a pattern similar to that observed for dG hydroxylation. Reaction of vanadium(IV) with H2O2 generated OH radicals, which were inhibited by DTPA and deferoxamine. Incubation of vanadium(IV) with dG or with DNA in the presence of H2O2 resulted in an enhanced 8-OHdG formation and substantial DNA strand breaks. Reaction of vanadium(IV) with t-butyl hydroperoxide generated hydroperoxide-derived free radicals, which caused 8-OHdG formation from dG and DNA strand breaks.

Chelating Agents↗

Chromium (IV)-mediated fenton-like reaction causes DNA damage: implication to genotoxicity of chromate.

This paper describes our deoxyribonucleic acid (DNA) damage and Fenton activity studies on Cr(IV) that were undertaken to examine a role of Cr(IV) in the biochemical mechanism of genotoxicity of Cr(VI) compounds. A Cr(IV)-containing compound, a Cr(IV)-ester, was synthesized and used as the first model compound for Cr(IV) studies. Electron spin resonance measurements demonstrated that in the presence of H2O2, this Cr(IV) compound acts as a potent Fenton-like reagent, i.e., it generates OH radical and a Cr(V) species (g = 1.9787) via: Cr(IV) + H2O2-->Cr(V) + OH + OH-. Measurements of OH yield as a function of H2O2 concentration showed that Cr(IV) is more potent than Cr(V) in generating OH. DNA damage assays demonstrate that Cr(IV) and the Cr(IV)/H2O2-generated OH radical can cause DNA strand breaks. The DNA damage caused by OH radical can be effectively blocked by OH radical scavengers. These results thus constitute the first direct evidence for DNA damage by Cr(IV) and Cr(IV)-mediated Fenton-like reaction and support the conjecture that Cr(IV) plays a significant role in the biochemical mechanism of the genotoxic reactions of Cr(VI) compounds and that this effect can be modulated by suitable antiradical agents.

Animals↗

Kidney cancer in Canada: the rapidly increasing incidence of adenocarcinoma in adults and seniors.

PURPOSE: To examine kidney cancer incidence and mortality patterns since 1969 in Canada. METHOD: Linear regression of the log rates was used to estimate secular trends by age group and sex, and age-period-cohort models were fitted to examine changes in kidney cancer and renal adenocarcinoma incidence rates. RESULTS: A substantial increase in incidence rates was observed among those 35 years and older, with average increases of 2.5% or more annually for both sexes. Age-period-cohort modelling suggested that much of this increase resulted from a period effect. Changes in mortality were much more modest, especially among those aged 0-34, for whom mortality rates actually declined by an average of 4.2% and 5.4% annually for males and females respectively. CONCLUSIONS: Kidney cancer incidence rates have increased significantly, especially renal adenocarcinoma among adults and seniors. Diagnostic improvements and increasing levels of obesity in the Canadian population may have contributed to these trends.

Adenocarcinoma↗