Distribution of blood and tissue concentrations in rats by inhalation exposure to 1,2-dichloroethane

Take, Makoto; Takanobu, Kenji; Takeuchi, Tetsuya; Haresaku, Mitsuru; Matsumoto, Michiharu; Nagano, Kasuke; Yamamoto, Seigo; Fukushima, Shoji

doi:10.1080/10934529.2013.773765

Cited by 8 publications

(5 citation statements)

References 16 publications

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“…Thus, we cannot precisely compare with the doses selected for our in vitro study with human exposure levels. However, according to results from a previous study (Take et al, ), the 1,2‐DCE concentration in the blood of rats exposed to 160 ppm 1,2‐DCE (650 mg m −3 ) was approximately 40 μ m . Moreover, concentrations of 1,2‐DCE in rat livers were greater than in the plasma, suggesting that 1,2‐DCE enrichment may occur in the liver.…”

Section: Discussionmentioning

confidence: 71%

Aberrant expression of miR‐451a contributes to 1,2‐dichloroethane‐induced hepatic glycerol gluconeogenesis disorder by inhibiting glycerol kinase expression in NIH Swiss mice

Zeng

Jiang

Fan

et al. 2017

J of Applied Toxicology

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The identification of aberrant microRNA (miRNA) expression during chemical-induced hepatic dysfunction will lead to a better understanding of the substantial role of miRNAs in liver diseases. 1,2-Dichloroethane (1,2-DCE), a chlorinated organic toxicant, can lead to hepatic abnormalities in occupationally exposed populations. To explore whether aberrant miRNA expression is involved in liver abnormalities mediated by 1,2-DCE exposure, we examined alterations in miRNA expression patterns in the livers of NIH Swiss mice after dynamic inhalation exposure to 350 or 700 mg m 1,2-DCE for 28 days. Using a microarray chip, we discovered that only mmumiR-451a was significantly upregulated in the liver tissue of mice exposed to 700 mg m 1,2-DCE; this finding was validated by quantitative real-time polymerase chain reaction. In vitro study revealed that it was metabolite 2-chloroacetic acid, not 1,2-DCE that resulted in the upregulation of mmu-miR-451a in the mouse AML12 cell line. Furthermore, our data showed that the upregulation of mmu-miR-451a induced by 2-chloroacetic acid could suppress the expression of glycerol kinase and lead to the inhibition of glycerol gluconeogenesis in mouse liver tissue and AML12 cells. These observations provide evidence that hepatic mmu-miR-451a responds to 1,2-DCE exposure and might induce glucose metabolism disorders by suppressing the glycerol gluconeogenesis process.

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Section: Discussionmentioning

confidence: 71%

Aberrant expression of miR‐451a contributes to 1,2‐dichloroethane‐induced hepatic glycerol gluconeogenesis disorder by inhibiting glycerol kinase expression in NIH Swiss mice

Zeng

Jiang

Fan

et al. 2017

J of Applied Toxicology

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“…1,2 To date, DCE exposure has been proved to have obvious toxic effects on the brain, liver, and kidney. In China, it is also used as a kind of solvent thinner of adhesives.…”

Section: Introductionmentioning

confidence: 99%

“…As an easily volatile solute, the main route of occupational exposure is inhalation through the respiratory route. 2,6,7 However, little is known about the mechanisms underlying DCE induced dysfunction of the kidney. 1,2 To date, DCE exposure has been proved to have obvious toxic effects on the brain, liver, and kidney.…”

Section: Introductionmentioning

confidence: 99%

“…Following absorption, DCE could rapidly distribute and accumulate in the blood, lung, liver, brain, kidney, and abdominal fat. 1,2 To date, DCE exposure has been proved to have obvious toxic effects on the brain, liver, and kidney. A line of evidence has proved that subacute exposure to DCE could obviously lead to severe toxic encephalopathy in both exposed workers 3 and mice.…”

Section: Introductionmentioning

confidence: 99%

“…4,5 Based on the data reported, DCE also causes toxicity of kidney, and several animal tests have showed that DCE resulted in an increase in the absolute and relative kidney weights and abnormal serological indexes. 2,6,7 However, little is known about the mechanisms underlying DCE induced dysfunction of the kidney.…”

Section: Introductionmentioning

confidence: 99%

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1,2-Dichloroethane induced nephrotoxicity through ROS mediated apoptosis in vitro and in vivo

Chen

et al. 2015

Toxicol. Res.

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Dichloroethane (DCE) is a ubiquitous occupational environmental contaminant. Subacute exposure of DCE could cause severe toxic encephalopathy. However, the toxicity of DCE on kidney and the molecular mechanism still remain elusive. To address this issue, we established a DCE-exposed animal model by inhalation in SD rats and used human embryonic kidney 293 (HEK293) cells in in vitro tests. We showed that the kidney/weight ratios were obviously higher in DCE-exposed groups than that in the control group. The renal distal tubules and distal convoluted tubule of rats treated with 577 ppm and 1000 ppm DCE obviously appeared abnormal. Moreover, apoptotic cells were found in the renal distal tubules from 1000 ppm DCE-exposed group. The antioxidant capacity was decreased and the levels of lipid peroxidation were increased in the kidney in exposure groups. In in vitro tests, we observed that there was no obvious toxicity in cells treated with DCE alone. However, over-expression of CYP2E1 or addition of S9 could remarkably increase the generation of ROS in HEK293 cells treated with DCE and decrease cell proliferation, even induce cell apoptosis. Antioxidant N-acetyl-L-cysteine (NAC) pre-treatment could inhibit the generation of ROS and alleviate cell apoptosis induced by DCE in the presence of an extra-metabolic system. Taken together, our findings provide direct evidence that excessive ROS generation may be the cause of the apoptosis effects induced by 1,2-dichloroethane on the kidney. † Electronic supplementary information (ESI) available. See

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Saturated Halogenated Aliphatic Hydrocarbons Two to Three Carbons

Bevan

2023

Patty's Toxicology

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The chemicals in this chapter are C 2 to C 3 aliphatic hydrocarbons containing, chlorine, bromine, or iodine. All are volatile liquids (flammable and nonflammable) at ambient temperatures, except for ethyl chloride (gas) and hexachloroethane (solid). Most, if not all, of the chemicals in this chapter are produced in closed‐system facilities, and the majority are used, primarily or exclusively, as intermediates or feedstocks to produce other chemicals. 1,1,1‐Trichloroethane is an ozone‐depleting substance and is tightly regulated under the Montreal Protocol on Substances that Deplete the Ozone Layer. Three chemicals were not included in this edition: 1,1,2,2‐tetrabromoethane, 1,2‐dibromo‐3‐chloropropane (DBCP), and ethyl iodide. DBCP has been effectively banned as a soil fumigant due to its well‐characterized toxicity, particularly on male reproduction. For the other two chemicals, the toxicity information and use are limited.

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Distribution of blood and tissue concentrations in rats by inhalation exposure to 1,2-dichloroethane

Cited by 8 publications

References 16 publications

Aberrant expression of miR‐451a contributes to 1,2‐dichloroethane‐induced hepatic glycerol gluconeogenesis disorder by inhibiting glycerol kinase expression in NIH Swiss mice

Aberrant expression of miR‐451a contributes to 1,2‐dichloroethane‐induced hepatic glycerol gluconeogenesis disorder by inhibiting glycerol kinase expression in NIH Swiss mice

1,2-Dichloroethane induced nephrotoxicity through ROS mediated apoptosis in vitro and in vivo

Saturated Halogenated Aliphatic Hydrocarbons Two to Three Carbons

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