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[Nickel exposure to A549 cell damage and L-ascorbic acid interference effect].

Yao Fu1, Yue Wang1, Han Dan1

  • 1School of Public Heath, Harbin Medical University, Harbin 150081, China.

Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi = Zhonghua Laodong Weisheng Zhiyebing Zazhi = Chinese Journal of Industrial Hygiene and Occupational Diseases
|December 15, 2015
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Summary
This summary is machine-generated.

Nickel smelting smoke damages lung cancer cells, increasing cell damage markers. L-ascorbic acid effectively protects against nickel-induced cell damage, showing significant protective effects.

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Area of Science:

  • Toxicology
  • Cell Biology
  • Environmental Health

Background:

  • Nickel smelting is a significant industrial process with potential health risks.
  • Human lung adenocarcinoma cells (A549) are a relevant model for studying carcinogenic effects.
  • Understanding the protective mechanisms against environmental toxins is crucial for public health.

Purpose of the Study:

  • To investigate the carcinogenic effects of varying nickel smelting smoke concentrations on A549 cells.
  • To evaluate the protective influence of L-ascorbic acid against nickel-induced cellular damage.
  • To analyze the impact of nickel exposure on intracellular calcium (Ca²⁺) and reactive oxygen species (ROS) levels, and HIF-1α gene expression.

Main Methods:

  • A549 cells were exposed to different concentrations of nickel refining dusts (0.00–100.00 µg/ml).
  • An intervention group received L-ascorbic acid (100 mmol/L) alongside nickel exposure.
  • Cell viability (MTT assay), Ca²⁺ concentration (Fluo-3 probe), ROS content (DCFH-DA), and HIF-1α gene expression (RT-PCR) were measured.

Main Results:

  • Nickel exposure increased cell growth inhibition, intracellular Ca²⁺, ROS content, and HIF-1α gene expression in a dose-dependent manner (P < 0.05).
  • L-ascorbic acid intervention significantly reduced these markers compared to the nickel-exposed group (P < 0.05).
  • These findings indicate L-ascorbic acid effectively mitigates nickel-induced cellular damage.

Conclusions:

  • Increased nickel concentration exacerbates damage to A549 cells.
  • L-ascorbic acid demonstrates a significant protective effect against nickel-induced cellular damage.
  • This study highlights the potential of L-ascorbic acid as a protective agent against nickel toxicity in lung adenocarcinoma cells.