Beryllium inhibits apoptosis via mitochondria in beryllium-induced lung disease in the rat

Exp Lung Res. 2019 Apr-May;45(3-4):92-100. doi: 10.1080/01902148.2019.1621409. Epub 2019 Jun 1.

Abstract

Objective: We aimed to determine whether beryllium toxicity was associated with mitochondria apoptosis pathway in SD rats. Methods: Thirty-two SD rats were given an intratracheal instillation dose of 10 g/l beryllium oxide (0.5 ml per rat). Additional 32 rats were given an intratracheal instillation dose of 0.9% normal saline (0.5 ml per rat). The percentage of apoptosis, mitochondrial membrane potential, the expression level of apoptosis related genes and proteins, including bcl2, Bax and Caspase-3 were detected. Results: The average of percentage of apoptosis, the expression of caspase-3, bax, and cytochrome c were decreased significantly in lung tissues from rats exposed to beryllium oxide compared to normal controls. The expression of bcl2 and ADP were increased significantly at 80 d after exposure. Conclusions: We conclude that inhibition of apoptosis by beryllium oxide involves mitochondrial apoptosis pathway in rat model of beryllium oxide-induced pulmonary disease.

Keywords: Beryllium; Sprague-Dawley rats; intratracheal instillation; mitochondria apoptosis pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Diphosphate / metabolism
  • Animals
  • Apoptosis / drug effects*
  • Beryllium / toxicity*
  • Caspase 3 / metabolism
  • Cytochromes c / metabolism
  • Lung Diseases / chemically induced
  • Lung Diseases / pathology*
  • Mitochondria / metabolism*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Rats

Substances

  • Bcl2 protein, rat
  • Proto-Oncogene Proteins c-bcl-2
  • beryllium oxide
  • Adenosine Diphosphate
  • Cytochromes c
  • Casp3 protein, rat
  • Caspase 3
  • Beryllium