4.7 Article

Potential pathway and mechanisms underlining the immunotoxicity of benzo[a]pyrene to Chlamys farreri

Journal

ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
Volume 30, Issue 43, Pages 97128-97146

Publisher

SPRINGER HEIDELBERG
DOI: 10.1007/s11356-023-29016-4

Keywords

B[a]P; Chlamys farreri; Immunotoxicity pathway; Metabolism; Neuroendocrine immunity; Apoptosis

Ask authors/readers for more resources

This study aims to investigate the effects of benzo(a)pyrene (B[a]P) on the immunity of Chlamys farreri and explore its potential molecular mechanism. Multiple biomarkers were used to assess these effects, and it was found that B[a]P had concentration-dependent immunotoxicity, possibly affecting immunity through the detoxification metabolic system, neuroendocrine system, and cell apoptosis pathway.
The long-distance migration of polycyclic aromatic hydrocarbons (PAHs) promotes their release into the marine environment, posing a serious threat to marine life. Studies have shown that PAHs have significant immunotoxicity effects on bivalves, but the exact mechanism of immunotoxicity remains unclear. This paper aims to investigate the effects of exposure to 0.4, 2, and 10 mu g/L of benzo(a)pyrene (B[a]P) on the immunity of Chlamys farreri under environmental conditions, as well as the potential molecular mechanism. Multiple biomarkers, including phagocytosis rate, metabolites, neurotoxicity, oxidative stress, DNA damage, and apoptosis, were adopted to assess these effects. After exposure to 0.4, 2, and 10 mu g/L B[a] P, obvious concentration-dependent immunotoxicity was observed, indicated by a decrease in the hemocyte index (total hemocyte count, phagocytosis rate, antibacterial and bacteriolytic activity). Analysis of the detoxification metabolic system in C. farreri revealed that B[a]P produced B[a]P-7,8-diol-9,10-epoxide (BPDE) through metabolism, which led to an increase in the expression of protein tyrosine kinase (PTK). In addition, the increased content of neurotransmitters (including acetylcholine, gamma-aminobutyric acid, enkephalin, norepinephrine, dopamine, and serotonin) and related receptors implied that B[a]P might affect immunity through neuroendocrine system. The changes in signal pathway factors involved in immune regulation indicated that B[a]P interfered with Ca2+ and cAMP signal transduction via the BPDE-PTK pathway or neuroendocrine pathway, resulting in immunosuppression. Additionally, B[a]P induced the increase in reactive oxygen species (ROS) content and DNA damage, as well as an upregulation of key genes in the mitochondrial pathway and death receptor pathway, leading to the increase of apoptosis rate. Taken together, this study comprehensively investigated the detoxification metabolic system, neuroendocrine system, and cell apoptosis to explore the toxic mechanism of bivalves under B[a]P stress.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available