Acute benzo[a]pyrene treatment causes different antioxidant response and DNA damage in liver, lung, brain, stomach

Chun Deng1, Fan Dang1, Jianghong Gao2

  • 1Department of Biological Science and Engineering, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi Province, 710049, China.

Heliyon
|November 21, 2018
PubMed

Insights

Acute benzo[a]pyrene (B[a]P) exposure causes oxidative stress and DNA damage in mice organs. The lung and liver showed the most significant damage, indicating B[a]P

Area of Science:

  • Toxicology
  • Environmental Health
  • Biochemistry

Background:

  • Benzo[a]pyrene (B[a]P) is a polycyclic aromatic hydrocarbon found in environmental pollutants.
  • The acute effects of B[a]P on oxidative stress and DNA damage across multiple organs are not fully understood.
  • Understanding these effects is crucial for assessing B[a]P's health risks.

Purpose of the Study:

  • To investigate the acute effects of B[a]P on oxidative stress and DNA damage in the liver, lung, stomach, brain, and kidney of ICR male mice.
  • To determine the time- and dose-dependent responses of antioxidant enzymes and oxidative stress markers.
  • To correlate biochemical findings with histopathological changes.

Main Methods:

  • Mice were administered varying doses of B[a]P acutely.
  • Body weight, antioxidant enzyme levels (SOD, CAT, GST, GPx), glutathione levels (GSH, GSSG), lipid peroxidation marker (MDA), and DNA damage were measured at 24 and 72 hours post-injection.
  • Serum markers of organ damage (GOT, GPT, BUN, creatinine) were analyzed.
  • Histopathological examination of organs was performed.

Main Results:

  • B[a]P treatment significantly decreased body weight.
  • Antioxidant enzymes showed complex time- and dose-dependent changes, with initial increases followed by decreases.
  • Markers of oxidative stress (MDA, GSSG) and DNA damage increased significantly in a time- and dose-dependent manner.
  • Organ damage predominance followed the order: lung > liver > kidney = stomach > brain, confirmed by histopathology.
  • Serum GOT, GPT, BUN, and creatinine levels were elevated.

Conclusions:

  • Acute B[a]P exposure disrupts antioxidant responses and exacerbates DNA damage in mice.
  • Different organs exhibit varying sensitivities to B[a]P-induced toxicity.
  • The lung and liver are particularly vulnerable to acute B[a]P insult.
  • Findings highlight the significant toxic potential of B[a]P even after acute exposure.

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