Bisphenol A induces apoptosis, oxidative stress and inflammatory response in colon and liver of mice in a mitochondria-dependent manner
Bisphenol A (BPA), a widely used industrial compound worldwide, was recently classified as an environmental toxicant. The intestines and liver are responsible for detoxification in humans and animals, and functional damage to these organs adversely affects the health of the body. However, the effect...
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doaj-42ccdc4c6b084825806d990b4e1cd69a2021-05-20T07:38:41ZengElsevierBiomedicine & Pharmacotherapy0753-33222019-09-01117Bisphenol A induces apoptosis, oxidative stress and inflammatory response in colon and liver of mice in a mitochondria-dependent mannerKai Wang0Zhenguo Zhao1Wu Ji2Department of General Surgery, Jinling Hospital, Nanjing Medical University, Nanjing, Jiangsu Provence, China; Department of Gastrointestinal Surgery, The Affiliated Hospital of Xuzhou Medical University, Jiangsu Provence, ChinaDepartment of General Surgery, The Affiliated Jiangyin Hospital of Southeast University Medical College, Jiangyin, Jiangsu Provence, ChinaDepartment of General Surgery, Jinling Hospital, Nanjing Medical University, Nanjing, Jiangsu Provence, China; Corresponding author.Bisphenol A (BPA), a widely used industrial compound worldwide, was recently classified as an environmental toxicant. The intestines and liver are responsible for detoxification in humans and animals, and functional damage to these organs adversely affects the health of the body. However, the effect of BPA on intestinal and liver function remains unclear. In this study, we investigated the effects of dietary BPA uptake on oxidative stress, inflammatory response, apoptosis and mitochondrial function in the colons and livers of mice. Dietary BPA uptake significantly reduced the body weights of mice as well as their colon and liver weights. Dietary BPA uptake increased the levels of oxidative stress indicators such as reactive oxygen species, reactive nitrogen species, malondialdehyde and hydrogen peroxide in mouse serum, colon and liver tissues. Antioxidant indicators, such as superoxide dismutase, glutathione peroxidase, catalase and total antioxidant capacity, as well as proinflammatory cytokines (interleukin-1β, interleukin-6, interleukin-8 and tumor necrosis factor-α) were also significantly reduced in the serum, colon, and liver tissues in the BPA group. Moreover, mitochondria-encoded genes and mitochondrial copy numbers were significantly reduced in the colon and liver tissues of the BPA mice. Dietary BPA uptake also increased gene abundance and enzyme activity of caspase-3, -8, -9 and -10. Our study found that dietary BPA induced oxidative stress, inflammatory response, apoptosis and mitochondrial dysfunction in mouse colons and livers.http://www.sciencedirect.com/science/article/pii/S0753332219323017Bisphenol AOxidative stressInflammatory responseApoptosisMitochondrial function |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Kai Wang Zhenguo Zhao Wu Ji |
spellingShingle |
Kai Wang Zhenguo Zhao Wu Ji Bisphenol A induces apoptosis, oxidative stress and inflammatory response in colon and liver of mice in a mitochondria-dependent manner Biomedicine & Pharmacotherapy Bisphenol A Oxidative stress Inflammatory response Apoptosis Mitochondrial function |
author_facet |
Kai Wang Zhenguo Zhao Wu Ji |
author_sort |
Kai Wang |
title |
Bisphenol A induces apoptosis, oxidative stress and inflammatory response in colon and liver of mice in a mitochondria-dependent manner |
title_short |
Bisphenol A induces apoptosis, oxidative stress and inflammatory response in colon and liver of mice in a mitochondria-dependent manner |
title_full |
Bisphenol A induces apoptosis, oxidative stress and inflammatory response in colon and liver of mice in a mitochondria-dependent manner |
title_fullStr |
Bisphenol A induces apoptosis, oxidative stress and inflammatory response in colon and liver of mice in a mitochondria-dependent manner |
title_full_unstemmed |
Bisphenol A induces apoptosis, oxidative stress and inflammatory response in colon and liver of mice in a mitochondria-dependent manner |
title_sort |
bisphenol a induces apoptosis, oxidative stress and inflammatory response in colon and liver of mice in a mitochondria-dependent manner |
publisher |
Elsevier |
series |
Biomedicine & Pharmacotherapy |
issn |
0753-3322 |
publishDate |
2019-09-01 |
description |
Bisphenol A (BPA), a widely used industrial compound worldwide, was recently classified as an environmental toxicant. The intestines and liver are responsible for detoxification in humans and animals, and functional damage to these organs adversely affects the health of the body. However, the effect of BPA on intestinal and liver function remains unclear. In this study, we investigated the effects of dietary BPA uptake on oxidative stress, inflammatory response, apoptosis and mitochondrial function in the colons and livers of mice. Dietary BPA uptake significantly reduced the body weights of mice as well as their colon and liver weights. Dietary BPA uptake increased the levels of oxidative stress indicators such as reactive oxygen species, reactive nitrogen species, malondialdehyde and hydrogen peroxide in mouse serum, colon and liver tissues. Antioxidant indicators, such as superoxide dismutase, glutathione peroxidase, catalase and total antioxidant capacity, as well as proinflammatory cytokines (interleukin-1β, interleukin-6, interleukin-8 and tumor necrosis factor-α) were also significantly reduced in the serum, colon, and liver tissues in the BPA group. Moreover, mitochondria-encoded genes and mitochondrial copy numbers were significantly reduced in the colon and liver tissues of the BPA mice. Dietary BPA uptake also increased gene abundance and enzyme activity of caspase-3, -8, -9 and -10. Our study found that dietary BPA induced oxidative stress, inflammatory response, apoptosis and mitochondrial dysfunction in mouse colons and livers. |
topic |
Bisphenol A Oxidative stress Inflammatory response Apoptosis Mitochondrial function |
url |
http://www.sciencedirect.com/science/article/pii/S0753332219323017 |
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