Association of hepatitis virus infection, alcohol consumption and plasma vitamin A levels with urinary 8-hydroxydeoxyguanosine in chemical workers

Wong, Roderick; Yeh, Chien-Yuh; Hsueh, Yu Mei; Wang, Jung‐Der; Yu, Lei; Cheng, Tsun‐Jen

doi:10.1016/s1383-5718(02)00294-2

Cited by 35 publications

(28 citation statements)

References 22 publications

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“…Previous findings revealed significant correlations between smoking and urinary 8-OHdG [32,33], in which urinary 8-OHdG reflected oxidative damage in lung tissue due to smoking. But two recent reports failed to replicate the association [34,35]. In the current study, smoking was only significantly associated with urinary 8-OHdG levels in electroplating workers.…”

Section: Discussioncontrasting

confidence: 86%

Chronic occupational exposure to hexavalent chromium causes DNA damage in electroplating workers

et al. 2011

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BackgroundOccupational exposure to chromium compounds may result in adverse health effects. This study aims to investigate whether low-level hexavalent chromium (Cr(VI)) exposure can cause DNA damage in electroplating workers.Methods157 electroplating workers and 93 control subjects with no history of occupational exposure to chromium were recruited in Hangzhou, China. Chromium levels in erythrocytes were determined by graphite furnace atomic absorption spectrophotometer. DNA damage in peripheral lymphocytes was evaluated with the alkaline comet assay by three parameters: Olive tail moment, tail length and percent of DNA in the comet tail (tail DNA%). Urinary 8-OHdG levels were measured by ELISA.ResultsChromium concentration in erythrocytes was about two times higher in electroplating workers (median: 4.41 μg/L) than that in control subjects (1.54 μg/L, P < 0.001). The medians (range) of Olive tail moment, tail length and tail DNA% in exposed workers were 1.13 (0.14-6.77), 11.17 (3.46-52.19) and 3.69 (0.65-16.20), and were significantly higher than those in control subjects (0.14 (0.01-0.39), 3.26 (3.00-4.00) and 0.69 (0.04-2.74), P < 0.001). Urinary 8-OHdG concentration was 13.65 (3.08-66.30) μg/g creatinine in exposed workers and 8.31 (2.94-30.83) μg/g creatinine in control subjects (P < 0.001). The differences of urinary 8-OHdG levels, Olive tail moment, tail length and tail DNA% between these two groups remained significant (P < 0.001) even after stratification by potential confounding factors such as age, gender, and smoking status. Chromium exposure was found to be positively associated with chromium levels in erythrocytes, urinary 8-OHdG levels, Olive tail moment, tail length and tail DNA%. Positive dose-response associations were also found between chromium levels in erythrocytes and Olive tail moment, tail length and tail DNA%.ConclusionThe findings in this study indicated that there was detectable chromium exposure in electroplating workers. Low-level occupational chromium exposure induced DNA damage.

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Section: Discussioncontrasting

confidence: 86%

Chronic occupational exposure to hexavalent chromium causes DNA damage in electroplating workers

et al. 2011

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“…By inducing hydroxylation of the C-8 position of 2Ј-deoxyguanosine, ROS produce 8-OHdG, which is stable and excreted in the urine without being metabolized (42). Hence, urinary 8-OHdG serves as a reliable biomarker of oxidative DNA damage in vivo (15,20,26,31,40). As expected, the urinary levels of 8-OHdG were markedly elevated in 20-wk-old WT mice maintained on the HF/HS diet for 12 wk.…”

Section: Discussionsupporting

confidence: 60%

Overexpression of human adiponectin in transgenic mice results in suppression of fat accumulation and prevention of premature death by high-calorie diet

Otabe

Yuan²,

Fukutani³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

122

116

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. Overexpression of human adiponectin in transgenic mice results in suppression of fat accumulation and prevention of premature death by high-calorie diet. Am J Physiol Endocrinol Metab 293: E210-E218, 2007. First published March 27, 2007 doi:10.1152/ajpendo.00645.2006.-Adiponectin, a physiologically active polypeptide secreted by adipocytes, shows insulin-sensitizing, anti-inflammatory, and antiatherogenic properties in rodents and humans. To assess the effects of chronic hyperadiponectinemia on metabolic phenotypes, we established three lines of transgenic mice expressing human adiponectin in the liver. When maintained on a high-fat/high-sucrose diet, mice of two lines that had persistent hyperadiponectinemia exhibited significantly decreased weight gain associated with less fat accumulation and smaller adipocytes in both visceral and subcutaneous adipose tissues. Macrophage infiltration in adipose tissue was markedly suppressed in the transgenic mice. Expression levels of adiponectin receptors were not altered in skeletal muscle or liver. Circulating levels of endogenous adiponectin were elevated, whereas fasting glucose, insulin, and leptin levels were reduced compared with control mice. In the hyperadiponectinemic mice daily food intake was not altered, but oxygen consumption was significantly greater, suggesting increased energy expenditure. Moreover, high-calorie diet-induced premature death was almost completely prevented in the hyperadiponectinemic mice in association with attenuated oxidative DNA damage. The transgenic mice also showed longer life span on a conventional low-fat chow. In conclusion, transgenic expression of human adiponectin blocked the excessive fat accumulation and reduced the morbidity and mortality in mice fed a high-calorie diet. These observations may provide new insights into the prevention and therapy of metabolic syndrome in humans.adipocyte; macrophage; life span; 8-hyroxy-2-deoxyguanosine RESTRICTION OF CALORIC INTAKE retards age-related changes and extends the maximum life span in mammals (22, 37). The longevity is associated with a reduction in steady-state oxidative damage to proteins, lipids, and DNA in animals subjected to restricted caloric intake (13). These decreases in oxidative damage may be attributable to a decrease in the mitochondrial free radical generation rate in various tissues (4). Conversely, obese rats fed a high-calorie diet ad libitum have a shorter life span than their lean counterparts fed a low-calorie diet (36). The excessive production of oxidative stress resulting from high caloric intake may play a role in the premature death.Metabolic syndrome associated with obesity is a growing cause of morbidity and mortality in humans (16, 18). Accumulating evidence has revealed that a reduction in the serum level of adiponectin, a bioactive peptide secreted by adipocytes, is involved in the development of metabolic syndrome and the acceleration of atherosclerosis. The serum level of adiponectin is decreased in patients with obesity (1), type 2 diabetes (17)...

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“…Thus, it is possible that the levels of oxidative DNA damage are reflective of different active diseases, especially active inflammation (Wong et al 2003). Besides, urinary levels of any oxidative lesion rely on efficient renal excretion of the damage products, so renal impairment can therefore affect urinary 8-OHdG levels (Akagi et al 2003).…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, the repair process for 8-OHdG–inflicted damage results in excised 8-OHdG adduct being excreted into the urine (Marnett 2000; Shigenaga et al 1989). Because of easy collection, urinary 8-OHdG is thus regarded as a suitable biomarker of oxidative stress (Toraason 1999; Wong et al 2003). …”

mentioning

confidence: 99%

Increased Levels of 8-Hydroxy-2′-Deoxyguanosine Attributable to Carcinogenic Metal Exposure among Schoolchildren

Wong

Kuo

Hsu

et al. 2005

Environ Health Perspect

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Arsenic, chromium, and nickel are reported in several epidemiologic studies to be associated with lung cancer. However, the health effects of arsenic, chromium, and nickel exposures are equivocal for children. Therefore, we performed a cross-sectional study to investigate possible associations between the internal concentrations of arsenic, chromium, and nickel and the level of oxidative stress to DNA in children. We measured urinary levels of arsenic, chromium, and nickel for 142 nonsmoking children using atomic absorption spectrometry. As a biomarker for oxidative stress, urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels were analyzed with an enzyme-linked immunosorbent assay kit. The median urinary 8-OHdG level for our subjects was 11.7 ng/mg creatinine. No obvious relationship between the levels of urinary nickel and 8-OHdG was found. Multiple linear regression analysis showed that children with higher urinary chromium had greater urinary 8-OHdG than did those with lower urinary chromium. Similarly, subjects with higher urinary arsenic had greater urinary 8-OHdG than did those with lower urinary arsenic. Furthermore, children with both high urinary arsenic and high urinary chromium had the highest 8-OHdG levels (mean ± SE, 16.0 ± 1.3; vs. low arsenic/low chromium, p < 0.01) in urine, followed by those with low arsenic/high chromium (13.7 ± 1.6; vs. low arsenic/low chromium, p = 0.25), high arsenic/low chromium (12.9 ± 1.6 vs. low arsenic/low chromium, p = 0.52), and low arsenic/low chromium (11.5 ± 1.3); the trend was significant (p < 0.001). Thus, environmental carcinogenic metal exposure to chromium and arsenic may play an important role in oxidative DNA damage to children.

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Association of hepatitis virus infection, alcohol consumption and plasma vitamin A levels with urinary 8-hydroxydeoxyguanosine in chemical workers

Cited by 35 publications

References 22 publications

Chronic occupational exposure to hexavalent chromium causes DNA damage in electroplating workers

Chronic occupational exposure to hexavalent chromium causes DNA damage in electroplating workers

Overexpression of human adiponectin in transgenic mice results in suppression of fat accumulation and prevention of premature death by high-calorie diet

Increased Levels of 8-Hydroxy-2′-Deoxyguanosine Attributable to Carcinogenic Metal Exposure among Schoolchildren

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