Lipid peroxidation and cell death mechanisms in rats and human cells induced by chloral hydrate

Y. S. Ho, H. Y. Ma, H. Y. Chang, B. L. Wei, C. C. Lee, S. Y. Ho, H. R. Guo, T. P. Wu, W. H. Chang, Y. J. Wang

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Chloral hydrate (CH) is widely used as a sedative and hypnotic in pediatric medicine. It is also a by-product of water chlorination and a metabolite of trichloroethylene. We examined the toxicological effects and cell death mechanisms of CH in rats and human Chang liver cells and lymphocytes. Monitoring of urinary 8-epi-PGF2α and serum levels of TNF-α served as index of lipid peroxidation and cytokine stimulation. The results indicated that a single intraperitoneal injection of 100 mg/kg CH in rats led to a nearly five-fold increase in urinary 8-epi-PGF2α on day 1, and a mild decrease on day 2 and day 3. The same treatment also induced significantly higher amounts of serum TNF-α on day 2 (about seven-fold). When the rats were treated with CH and vitamin E simultaneously, the amount of urinary 8-epi-PGF2α and serum TNF- were significantly lower than that in the rats treated with CH alone. CH caused a greater cytotoxic effect in human Chang liver cells than in comparison with lymphocytes. After treatment with CH, apoptosis features were observed in human lymphocytes, but not Chang liver cells. CH-induced cell damage in lymphocytes may offer signals for the induction of caspases activation. Further studies are needed to evaluate the relationship between caspases activation and the cleavage of other death substrates during postmitotic apoptosis in human lymphocytes.

Original languageEnglish
Pages (from-to)621-629
Number of pages9
JournalFood and Chemical Toxicology
Volume41
Issue number5
DOIs
Publication statusPublished - May 1 2003

Fingerprint

chloral hydrate
Chloral Hydrate
Cell death
Lipid Peroxidation
Rats
cell death
lipid peroxidation
Cell Death
Cells
Lymphocytes
Lipids
rats
lymphocytes
Dinoprost
Liver
cells
hepatocytes
caspases
Caspases
apoptosis

Keywords

  • 8-Epi-prostaglandin F2α
  • Cell death mechanisms
  • Chloral hydrate
  • Lipid peroxidation
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Food Science
  • Toxicology

Cite this

Lipid peroxidation and cell death mechanisms in rats and human cells induced by chloral hydrate. / Ho, Y. S.; Ma, H. Y.; Chang, H. Y.; Wei, B. L.; Lee, C. C.; Ho, S. Y.; Guo, H. R.; Wu, T. P.; Chang, W. H.; Wang, Y. J.

In: Food and Chemical Toxicology, Vol. 41, No. 5, 01.05.2003, p. 621-629.

Research output: Contribution to journalArticle

Ho, YS, Ma, HY, Chang, HY, Wei, BL, Lee, CC, Ho, SY, Guo, HR, Wu, TP, Chang, WH & Wang, YJ 2003, 'Lipid peroxidation and cell death mechanisms in rats and human cells induced by chloral hydrate', Food and Chemical Toxicology, vol. 41, no. 5, pp. 621-629. https://doi.org/10.1016/S0278-6915(02)00323-X
Ho, Y. S. ; Ma, H. Y. ; Chang, H. Y. ; Wei, B. L. ; Lee, C. C. ; Ho, S. Y. ; Guo, H. R. ; Wu, T. P. ; Chang, W. H. ; Wang, Y. J. / Lipid peroxidation and cell death mechanisms in rats and human cells induced by chloral hydrate. In: Food and Chemical Toxicology. 2003 ; Vol. 41, No. 5. pp. 621-629.
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AB - Chloral hydrate (CH) is widely used as a sedative and hypnotic in pediatric medicine. It is also a by-product of water chlorination and a metabolite of trichloroethylene. We examined the toxicological effects and cell death mechanisms of CH in rats and human Chang liver cells and lymphocytes. Monitoring of urinary 8-epi-PGF2α and serum levels of TNF-α served as index of lipid peroxidation and cytokine stimulation. The results indicated that a single intraperitoneal injection of 100 mg/kg CH in rats led to a nearly five-fold increase in urinary 8-epi-PGF2α on day 1, and a mild decrease on day 2 and day 3. The same treatment also induced significantly higher amounts of serum TNF-α on day 2 (about seven-fold). When the rats were treated with CH and vitamin E simultaneously, the amount of urinary 8-epi-PGF2α and serum TNF- were significantly lower than that in the rats treated with CH alone. CH caused a greater cytotoxic effect in human Chang liver cells than in comparison with lymphocytes. After treatment with CH, apoptosis features were observed in human lymphocytes, but not Chang liver cells. CH-induced cell damage in lymphocytes may offer signals for the induction of caspases activation. Further studies are needed to evaluate the relationship between caspases activation and the cleavage of other death substrates during postmitotic apoptosis in human lymphocytes.

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