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Original Articles
- Effects of Ethanol and Phenobarbital on Hemoglobin Adducts Formation in Rats Exposed to Direct Black 38.
- Chi Nyon Kim, Se Hoon Lee, Jaehoon Roh
- Korean J Prev Med. 2002;35(3):229-235.
- 14,825 View
- 22 Download
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Abstract
PDF - OBJECTIVES
To evaluate the effects on the formation of benzidine-hemoglobin, and benzidine metabolite-hemoglobin adducts, caused by pretreatment with the known xenobiotic metabolism effectors, ethanol and phenobarbital, in rats administered Direct Black 38 dye. METHODS: The experimental rats were divided into three groups: a control group, an ethanol group and a phenobarbital group. Rats were pretreated with ethanol (1g/kg) or phenobarbital (80mg/kg) 24 hours prior to the oral administration of Direct Black 38 (0.5mmol/kg), with the control group being administered the same amount of distilled water. Blood samples were obtained from the vena cava of 5 rats from each group prior to, and at 30 min, 3 h, 6 h, 9 h, 12 h, 24 h, 48 h, 72 h, 96 h, and 144 h following the oral administration of Direct Black 38. Directly after sampling the blood was separated into hemoglobin and plasma, with the adducts being converted into aromatic amines by basic hydrolysis. Hydrolyzed benzidiene, monoacetylbenzidine and 4-aminobiphenyl were analyzed by reverse-phase liquid chromatography with an electrochemical detector. The quantitative amount of the metabolites was expressed by the hemoglobin binding index (HBI). RESULTS: In the ethanol group, benzidine-, monoacetylben-zidine-, and 4-aminobiphenyl-HBI were increased to a greater extent than those in the control group. These results were attributed to the ethanol inducing N-hydroxylation, which is related to the formation of the hemoglobin adduct. In the phenobarbital group, all the HBIs, with the exception of the benzidine-HBI, were increased to a greater extent than those of the control group. These results were attributed to the phenobarbital inducing N-hydroxylation related to the formation of the hemoglobin adduct. The N-acetylation ratio was only increased with the phenobarbital pretreatment due to the lower benzidine-HBI of the phenobarbital group compared to those of the control and ethanol groups. The N-acetylation ratios for all groups were higher than 1 for the duration of the experimental period. Although the azo reduction was unaffected by the ethanol, it was inhibited by the phenobarbital. The ratio of the benzidine-HBI in the phenobarbital group was lower than those of the ethanol the control groups for the entire experiment. CONCLUSION: Our results indicate that both ethanol and phenobarbital increase the formation of adducts by the induction of N-hydroxylation, but also induced N-acetylation. Phenobarbital decreased the formation of benzidine-HBI due to the decrease of the azo reduction. These results suggest that the effects of ethanol and phenobarbital need to be considered in the biochemical monitoring of Direct Black 38. -
Summary
- Hematuria among Benzidine Dye Industry Workers.
- Mi A Son, Domyung Paek, Jung Kun Choi, Su Kyeong Park, Jung Soon Park, Se Min Oh, Jung Sun Park, Dong Ook Park
- Korean J Prev Med. 1995;28(1):225-243.
- 2,351 View
- 24 Download
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Abstract
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- Benzidine Industry in Korea has started after Japan has banned its production in early 1970's. and it has been in operation in Korea for over 20 years. However, it is not known yet whether any bladder cancer has developed from benzidine exposure. This study was done to screen benzidine-exposed workers for bladder cancer, and to examine the feasibility of employing screening test at the workplace. All the workplaces that manufacture or use benzidine for more than 20 years in Korea have been covered in this study, and they include 2 benzidine manufacturing factories, 5 benzidine using factories, as well as 2 benzidine free factories as an outside control. In total, 516 workers were screened with urine stick test and urine cytology test for the evidence of hematuria and abnormal urothelial cells. Each worker was also asked about risk factors and symptoms of bladder cancer including past medical history, smoking, medication and occupational history. Benzidine in the air was measured by personal and area sampling. Out of 516 screened workers, 84(16.3%)workers showed positive hematuria in urine stick test, and 7(1.4%)workers showed degenerative cells in urine cytology tests. Those workers with abnormal urine test results who have been exposed to benzidine for more than 10 years were further screened, and, in total. 23 workers were examined with intra-venous pyelography and cystoscopy. None of those screened had any evidence of bladder cancer. When workers with only past hematuria history were included in the positive hematuria group, 96(18.5%) had positive hematuria. On the multiple logistic regression analysis, positive hematuria was significantly associated with benzidine exposure history of other occupations with elevated bladder cancer risk, pyuria and glycosuria. The association got stronger as direct benzidine exposure was accounted through individual task analysis, and as exposure duration was accounted with tenure analysis. For those with benzidine exposure with more than 10 years of tenure, the odds of having positive hematuria was elevated 2.14(95%C.I is 1.08 to 4.25) times more than for those without exposure. Even though bladder cancer was not detected for several limitations including short observation period, majority of studied workers with short latency, healthy worker effect, and low sensitivity of single screening test in a cross-sectional study, the study results suggest that hematuria screening is a feasible and very useful test for bladder cancer screening among benzidine exposed workers.
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Summary
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