Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2024 Jul 6;25(13):7420.
doi: 10.3390/ijms25137420.

Liver and Pancreatic Toxicity of Endocrine-Disruptive Chemicals: Focus on Mitochondrial Dysfunction and Oxidative Stress

Adina V Lința  1   2   3 , Bogdan M Lolescu  2   3 , Cosmin A Ilie  2   4 , Mihaela Vlad  5 , Alexandru Blidișel  6   7 , Adrian Sturza  1   2 , Claudia Borza  1   2 , Danina M Muntean  1   2 , Octavian M Crețu  6   7
Affiliations
Review

Liver and Pancreatic Toxicity of Endocrine-Disruptive Chemicals: Focus on Mitochondrial Dysfunction and Oxidative Stress

Adina V Lința et al. Int J Mol Sci. .

Abstract

In recent years, the worldwide epidemic of metabolic diseases, namely obesity, metabolic syndrome, diabetes and metabolic-associated fatty liver disease (MAFLD) has been strongly associated with constant exposure to endocrine-disruptive chemicals (EDCs), in particular, the ones able to disrupt various metabolic pathways. EDCs have a negative impact on several human tissues/systems, including metabolically active organs, such as the liver and pancreas. Among their deleterious effects, EDCs induce mitochondrial dysfunction and oxidative stress, which are also the major pathophysiological mechanisms underlying metabolic diseases. In this narrative review, we delve into the current literature on EDC toxicity effects on the liver and pancreatic tissues in terms of impaired mitochondrial function and redox homeostasis.

Keywords: endocrine disruptors; liver; metabolism-disrupting chemicals; mitochondrial dysfunction; oxidative stress; pancreas.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Mechanisms of liver and pancreatic EDC-related mitochondrial toxicity. Created with BioRender. Δψm = mitochondrial membrane potential; ATP = adenosine triphosphate; DNA = deoxyribonucleic acid; ROS = reactive oxygen species; ↑ = increased; ↓ = decreased.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

References

    1. Lopez-Jimenez F., Almahmeed W., Bays H., Cuevas A., Di Angelantonio E., le Roux C.W., Sattar N., Sun M.C., Wittert G., Pinto F.J., et al. Obesity and cardiovascular disease: Mechanistic insights and management strategies. A joint position paper by the World Heart Federation and World Obesity Federation. Eur. J. Prev. Cardiol. 2022;29:2218–2237. doi: 10.1093/eurjpc/zwac187. - DOI - PubMed
    1. Preda A., Carbone F., Tirandi A., Montecucco F., Liberale L. Obesity phenotypes and cardiovascular risk: From pathophysiology to clinical management. Rev. Endocr. Metab. Disord. 2023;24:901–919. doi: 10.1007/s11154-023-09813-5. - DOI - PMC - PubMed
    1. Schwartz M.W., Seeley R.J., Zeltser L.M., Drewnowski A., Ravussin E., Redman L.M., Leibel R.L. Obesity Pathogenesis: An Endocrine Society Scientific Statement. Endocr. Rev. 2017;38:267–296. doi: 10.1210/er.2017-00111. - DOI - PMC - PubMed
    1. Papalou O., Kandaraki E.A., Papadakis G., Diamanti-Kandarakis E. Endocrine Disrupting Chemicals: An Occult Mediator of Metabolic Disease. Front. Endocrinol. 2019;10:112. doi: 10.3389/fendo.2019.00112. - DOI - PMC - PubMed
    1. Brown R.E., Sharma A.M., Ardern C.I., Mirdamadi P., Mirdamadi P., Kuk J.L. Secular differences in the association between caloric intake, macronutrient intake, and physical activity with obesity. Obes. Res. Clin. Pract. 2016;10:243–255. doi: 10.1016/j.orcp.2015.08.007. - DOI - PubMed

Substances

LinkOut - more resources