Long-chain chlorinated paraffins (LCCPs) exposure induces apoptosis in primary chicken embryo hepatocytes through oxidative stress

Long-chain chlorinated paraffins (LCCPs) are industrial raw materials extensively utilized worldwide. Recently, their environmental impact has escalated, exacerbating challenges in animal husbandry and contributing to pollution from the food industry, which poses certain risks to animal growth and development. However, the toxicological effects of LCCPs exposure on poultry remain inadequately understood. The liver is a critical organ in poultry, serving not only as the largest digestive gland but also as the center of metabolism. Consequently, this study employed primary chicken embryo hepatocyte as a model to investigate the toxicological effects of LCCPs exposure and its potential mechanisms of action. Our findings indicate that the proliferation capacity of primary chicken embryo hepatocytes exposed to LCCPs at concentrations of 1, 10, and 100 μg/L was significantly diminished, with an observed arrest in the G0/G1 phase and a notable reduction in the proportion of cells in the G2/M phase. Additionally, we observed that LCCPs exposure markedly decreased the autophagy levels in primary chicken embryo hepatocytes while significantly increase the levels of apoptosis. To elucidate the molecular mechanisms underlying LCCP-induced apoptosis in these cells, we assessed oxidative stress levels (ROS) and mitochondrial membrane potential, and found that the level of ROS was significantly increased, and the level of mitochondrial membrane potential was significantly decreased in primary chicken embryo hepatocytes after exposure to LCCPs. To further clarify whether LCCPs induced apoptosis in primary chicken embryo hepatocytes through oxidative stress, oxidative stress inhibitors (NAC) were used, and it was found that apoptosis caused by LCCPs exposure was significantly alleviated. These data suggest that LCCPs exposure could induce apoptosis in primary chicken embryo hepatocytes through oxidative stress. In conclusion, the current work shows that LCCPs have multiple toxic effects on primary chicken embryo hepatocytes, and lays a theoretical foundation for future research on the harmful effects of LCCPs in the poultry industry.

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Publication Details

Journal
Ecotoxicology and Environmental Safety
Published
2024-12-20
DOI
https://doi.org/10.1016/j.ecoenv.2024.117566
Citations
4
Primary Topic
Toxic Organic Pollutants Impact
Type
article
Field-Weighted Citation Impact
1.26

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article

Long-chain chlorinated paraffins (LCCPs) exposure induces apoptosis in primary chicken embryo hepatocytes through oxidative stress

Guoxia Wang, Xin Zheng, Haochu Deng, Yuebing Kong et al.
4 citations
Ecotoxicology and Environmental Safety
Toxic Organic Pollutants Impact
1.26
article

Long-chain chlorinated paraffins (LCCPs) exposure induces apoptosis in primary chicken embryo hepatocytes through oxidative stress

Guoxia Wang, Xin Zheng, Haochu Deng, Yuebing Kong, Ruoting Zhang, Yezi Taishi
article en
4 citations

Abstract

Long-chain chlorinated paraffins (LCCPs) are industrial raw materials extensively utilized worldwide. Recently, their environmental impact has escalated, exacerbating challenges in animal husbandry and contributing to pollution from the food industry, which poses certain risks to animal growth and development. However, the toxicological effects of LCCPs exposure on poultry remain inadequately understood. The liver is a critical organ in poultry, serving not only as the largest digestive gland but also as the center of metabolism. Consequently, this study employed primary chicken embryo hepatocyte as a model to investigate the toxicological effects of LCCPs exposure and its potential mechanisms of action. Our findings indicate that the proliferation capacity of primary chicken embryo hepatocytes exposed to LCCPs at concentrations of 1, 10, and 100 μg/L was significantly diminished, with an observed arrest in the G0/G1 phase and a notable reduction in the proportion of cells in the G2/M phase. Additionally, we observed that LCCPs exposure markedly decreased the autophagy levels in primary chicken embryo hepatocytes while significantly increase the levels of apoptosis. To elucidate the molecular mechanisms underlying LCCP-induced apoptosis in these cells, we assessed oxidative stress levels (ROS) and mitochondrial membrane potential, and found that the level of ROS was significantly increased, and the level of mitochondrial membrane potential was significantly decreased in primary chicken embryo hepatocytes after exposure to LCCPs. To further clarify whether LCCPs induced apoptosis in primary chicken embryo hepatocytes through oxidative stress, oxidative stress inhibitors (NAC) were used, and it was found that apoptosis caused by LCCPs exposure was significantly alleviated. These data suggest that LCCPs exposure could induce apoptosis in primary chicken embryo hepatocytes through oxidative stress. In conclusion, the current work shows that LCCPs have multiple toxic effects on primary chicken embryo hepatocytes, and lays a theoretical foundation for future research on the harmful effects of LCCPs in the poultry industry.

Ecotoxicology and Environmental SafetyVol. 290
Jilin University (CN), First Hospital of Jilin University (CN), Jilin Agricultural University (CN)
National Natural Science Foundation of China
Zero hunger
Openalex Percentile: Top 20%
Toxic Organic Pollutants Impact
1.26
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