Annals of Occupational and Environmental Medicine

Original Article

Acute Toxicity of Arsenic in Rats and Mice: Byung Sun Choi, Dae Woong Kang, Jin Young Lee, Eon Sub Park, Yeon Pyo Hong, Ji Sun Yang, Hyomin Lee, Jung Duck Park; Korean Journal of Occupational and Environmental Medicine 2003;15(4):323-334. Published online December 31, 2003; DOI: https://doi.org/10.35371/kjoem.2003.15.4.323

OBJECTIVES
Arsenic (As) is ubiquitously distributed in the environment and is known as a human carcinogen. In this study, acute As toxicity at lethal dosage in rats and mice was evaluated, and As-induced hepatotoxicity was characterized.
METHODS
Male Sprague-Dawley rats, male ICR mice and trivalent inorganic As, sodium arsenite, were used in this experiment. LD50 and LD100 were calculated from 24-hour lethality after the single subcutaneous administration of As into rats and mice. Serum and liver were collected from the surviving animals. The activities of ALT, AST and gamma-GT in serum were determined, and the concentrations of MDA, GSH and CYP450 in liver were analyzed.
RESULTS
The LD50 and LD100 of sodium arsenite were calculated as 12 mg/kg and 13 mg/kg for rats, and 16.5 mg/kg and 19 mg/kg for mice, respectively. Thus, the rat was more susceptible than the mouse to the acute lethal toxicity of As. The histopathological changes induced by As were similar between rats and mice. AST was increased in high-dose As-treated rats and mice, whereas ALT was increased in high-dose As-treated mice but not in rats. gamma-GT was not significantly changed between the two animal groups. As increased lipid peroxidation, but decreased GSH and CYP450 in the liver of both rats and mice, in dose-dependent patterns. These results indicate that oxidative stress might be one of the mechanisms in As-induced hepatotoxicity.
CONCLUSION
Rats were more susceptive than mice to acute As toxicity, and oxidative stress might play a part in liver injury induced by As.

Citations

Citations to this article as recorded by

Intestinal microbiota dysbiosis contributed to the development of subchronic liver damage in arsenic-exposed mice
Ling Dong, Peng Luo, Aihua Zhang*
Acta Biochimica et Biophysica Sinica.2024;[Epub] CrossRef
Oral arsenite exposure induces inflammation and apoptosis in pulmonary tissue: acute and chronic evaluation in young and adult mice
Samata Pradhan, Syed Afroz Ali, Mahesh Rachamalla, Som Niyogi, Ashok Kumar Datusalia
BioMetals.2024; 37(3): 587. CrossRef
The Protective Effects of Trametes Versicolor on Arsenic-Induced Male Reproductive Toxicity through Regulation of Oxidative Stress: A Biochemical and Histopathological Survey
Fatemeh Solaimani, Emran Habibi, Maryam Ghasemi, Saba Mahboubi, Ehsan Zamani, Fatemeh Shaki, R. Henkel
Andrologia.2023; 2023: 1. CrossRef
Thermal effects on antioxidant enzymes response in Tilapia, Oreochromis niloticus exposed Arsenic
EunYoung Min, Ji Won Jeong, Ju-Chan Kang
Journal of fish pathology.2014; 27(2): 115. CrossRef
Monitoring Heavy Metals in Meat and Meat Products
Tae-Ik Hwang, Tae-Hyun Ahn, Eun-Jung Kim, Jung-Ah Lee, Myoung-Hee Kang, Young-Mi Jang, Mee-Hye Kim
Korean Journal of Food Science and Technology.2011; 43(5): 525. CrossRef

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Original Article

Hepatic Effect of Simultaneous Exposure to Nickel and Cadmium in Rats: Bong Suk Cha, Seungjun Wang, Sei Jin Chang; Korean Journal of Occupational and Environmental Medicine 2000;12(1):111-118. Published online March 31, 2000; DOI: https://doi.org/10.35371/kjoem.2000.12.1.111

Abstract PDF: OBJECTIVES
This research was intended to verify hepatic effect of simutaneously combined exposure of nickel chloride and cadmium chloride with IPRL(Isolated Perfused Rat Liver) method.
METHODS
AST(aspartate aminotransferase), ALT(alanine aminotransferase), LDH(lactate dehydrogenase) and perfusion flow rate were used as the indicator of hepatotoxicity and oxygen consumption rate were used as the indicator of viability. 300(+/-50) g weighted rats were allocated randomly to each group (control group, 50 microM 200 microM separately exposure group of NiC1, and CdC1, simultaneously combined exposure group of NiC1 and CdC1) by 5, totally 35. Buffer which got out of liver was sampled and then biochemical indicator of hepatotoxicity was measured. In order to verify difference among groups, two way repeated ANOVA was used. With comparing mean summation of separate exposure group with mean of simultaneous exposure group, possibility that combined effect could be synergistic effect was verified.
RESULTS
AST, ALT, LDH increased in both of separate exposure group and simultaneous exposure group. Perfusion flow rate and oxygen consumption rate decreased but statistically significant difference among groups was not found, In each exposure group, AST, ALT, LDH, oxygen consumption rate of simultaneous exposure group increased more than sum of separate exposure group after any sampling time.
CONCLUSIONS
It was found that simultaneous combined effect could be synergistic effect through the biochemical indicator of hepatotoxicity.

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Original Article

The Metabolism and Liver Toxicity of N, N-dimethylformamide in the Isolated Perfused Liver: Sang Baek Koh, Bong Suk Cha, Myung Guen Kang, Sang Yeol Koh, Jung Woo Lee, Sang Ok Kwon; Korean Journal of Occupational and Environmental Medicine 1997;9(2):217-229. Published online June 30, 1997; DOI: https://doi.org/10.35371/kjoem.1997.9.2.217

Abstract PDF

N, N-dimethylformamide (DMF) is a solvent which is widely used in the industrial workplace. It causes the liver damages to the chronically exposed workers and is also well known as the harzadous material to generate occupational malignancies. DMF is mainly metabolized into N-hydroxymethyl-N-methylformamide (HMMF) by the microsomal cytochrome p-450. HMMF breaks down to NMF. However, the detailed mechanism of its toxicity are unknown. In this experiment, the metabolism and the toxicity of DMF was investigated using an isolated perfumed liver model. DMF (0, 10, 25mM) were added into recirculating perfusate of the isolated perfused rat liver. Samples were collected at 0, 30, 45, 60, 75, 90 minutes from inferior vena cava. The gas-chromatography was used to analyze the metabolite of DMF, The changes in the oxygen consumption rate by DMF were monitored during perfusion. The enzyme activity (AST, ALT, LDH) in the perfusate were treasured to find out whether DMF causers hepatotoxicity. As perfusion continued, DMF concentration in the perfusate decreased, and NMF 1.16mM was detected. The oxygen consumption rate increased both at 10mM and 25mM DMF concentration. However, when SKF 525A, a known inhibitor of cytochrome p-450, had been pretreated (300uM before DMF addition, the oxygen consumption rate was significantly inhibited, indicating that cytochrome p-450 system is responsible for the conversion to NMF. With DMF addition, the activity of AST, ALT, and LDH significantly increased time dependently and dose dependently. However, the pretreatment of perfused liver with SKF 525A shoved that the release of AST, ALT and LDH was inhibited. In summary, it is found that DMF is metabolized to NMF in liver, and that cytochrome p-450 mono-oxygenase is suggested to play a role in the biotransformation of NMF. The time course of BMF toxicity in relation to NMF formation is compatible with hypothesis that the hepatotoxicity of DMF is mediated via NMF. Further study combined with in vivo experiment through the toxicological approaches is expected.

Citations

Citations to this article as recorded by

Clinical Outcomes of Occupational Exposure to N,N-Dimethylformamide: Perspectives from Experimental Toxicology
Tae Hyun Kim, Sang Geon Kim
Safety and Health at Work.2011; 2(2): 97. CrossRef

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