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[Mechanisms of apoptosis induced by trichloroethylene in normal human epidermis keratinocytes]

Tong Shen1, Tai Ma, Liang-ping Ye

  • 1Department of Toxicology, School of Public Health, Anhui Medical University, Hefei 230032, China.

Zhonghua Yi Xue Za Zhi
|March 3, 2010
PubMed
Abstract

Insights

Trichloroethylene (TCE) exposure induces apoptosis in human skin cells via the intrinsic mitochondrial pathway. This involves decreased mitochondrial membrane potential and caspase-9-dependent caspase-3 activation, highlighting a key mechanism of TCE toxicity.

Area of Science:

  • Toxicology
  • Cell Biology
  • Dermatology

Background:

  • Trichloroethylene (TCE) is a common industrial solvent with known toxic effects.
  • Understanding the cellular mechanisms of TCE toxicity is crucial for risk assessment and prevention.
  • Apoptosis, or programmed cell death, is a key cellular response to toxic insults.

Purpose of the Study:

  • To elucidate the mechanism of trichloroethylene (TCE)-induced apoptosis in normal human epidermis keratinocytes (NHEK).
  • To investigate the roles of Caspase activities and mitochondrial membrane potential (ΔPsim) in TCE-induced apoptosis.

Main Methods:

  • Normal human epidermis keratinocytes (NHEK) were exposed to varying concentrations of TCE.
  • Caspase-3, -8, and -9 activities were measured using commercial assay kits.
  • Apoptosis and mitochondrial membrane potential (ΔPsim) were assessed by flow cytometry.
  • Inhibitors of Caspase-3 and -9 were used to verify the apoptotic pathway.

Main Results:

  • TCE exposure dose- and time-dependently increased Caspase-3 and Caspase-9 activities, but not Caspase-8.
  • TCE significantly induced apoptosis and decreased mitochondrial membrane potential (ΔPsim) in NHEK cells.
  • Inhibitor studies confirmed that Caspase-9 activation is upstream of Caspase-3 activation in TCE-induced apoptosis.

Conclusions:

  • TCE induces apoptosis in NHEK cells through the intrinsic mitochondrial pathway.
  • The mechanism involves a decrease in ΔPsim and subsequent Caspase-9-dependent activation of Caspase-3.
  • This study clarifies a critical cellular mechanism underlying TCE dermatotoxicity.

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