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
. 2022 Oct 1;12(10):1405.
doi: 10.3390/biom12101405.

The Credible Role of Curcumin in Oxidative Stress-Mediated Mitochondrial Dysfunction in Mammals

Affiliations
Review

The Credible Role of Curcumin in Oxidative Stress-Mediated Mitochondrial Dysfunction in Mammals

Muthuswamy Sathyabhama et al. Biomolecules. .

Abstract

Oxidative stress and mitochondrial dysfunction are associated with the pathogenesis of several human diseases. The excessive generation of reactive oxygen species (ROS) and/or lack of adequate antioxidant defenses causes DNA mutations in mitochondria, damages the mitochondrial respiratory chain, and alters membrane permeability and mitochondrial defense mechanisms. All these alterations are linked to the development of numerous diseases. Curcumin, an active ingredient of turmeric plant rhizomes, exhibits numerous biological activities (i.e., antioxidant, anti-inflammatory, anticancer, and antimicrobial). In recent years, many researchers have shown evidence that curcumin has the ability to reduce the oxidative stress- and mitochondrial dysfunction-associated diseases. In this review, we discuss curcumin's antioxidant mechanism and significance in oxidative stress reduction and suppression of mitochondrial dysfunction in mammals. We also discuss the research gaps and give our opinion on how curcumin research in mammals should proceed moving forward.

Keywords: anti-inflammatory; anticancer; antimicrobial; antioxidant; curcumin; mammals; mitochondrial dysfunction; oxidative stress.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Molecular targets and antioxidant mechanism of curcumin. The activities of superoxide dismutases (SOD), catalase (CAT), reactive oxygen species (ROS), malondialdehyde (MDA), glutathione S-transferases (GST), and glutathione peroxidase (GPx) adapted from [39,40,44,45].
Figure 2
Figure 2
Role of curcumin in reducing mitochondrial dysfunction in various organs: in the brain—Alzheimer’s disease; eye—retinal infection; skeletal system; liver function; kidney disease, and lymphocyte regulation. Curcumin mainly regulates ROS levels and maintains the antioxidant system for proper regulation of mitochondrial function. (APP—amyloid precursor protein; EGF—epidermal growth factor; HO-1—Heme oxygenase 1; NQO1—NAD(P)H quinone oxidoreductase 1; Nrf2—nuclear factor erythroid 2-related factor 2; Keap1—Kelch-like ECH-associated protein 1; ARE—antioxidant response element.).

Similar articles

Cited by

References

    1. Duchen M.R. Mitochondria and Calcium: From Cell Signalling to Cell Death. J. Physiol. 2000;529:57–68. doi: 10.1111/j.1469-7793.2000.00057.x. - DOI - PMC - PubMed
    1. Andersson S.G.E., Zomorodipour A., Andersson J.O., Sicheritz-Pontén T., Alsmark U.C.M., Podowski R.M., Näslund A.K., Eriksson A.-S., Winkler H.H., Kurland C.G. The Genome Sequence of Rickettsia Prowazekii and the Origin of Mitochondria. Nature. 1998;396:133–140. doi: 10.1038/24094. - DOI - PubMed
    1. Anderson S., Bankier A.T., Barrell B.G., de Bruijn M.H.L., Coulson A.R., Drouin J., Eperon I.C., Nierlich D.P., Roe B.A., Sanger F., et al. Sequence and Organization of the Human Mitochondrial Genome. Nature. 1981;290:457–465. doi: 10.1038/290457a0. - DOI - PubMed
    1. Santorelli F.M., Shanske S., Macaya A., DeVivo D.C., DiMauro S. The Mutation at Nt 8993 of Mitochondrial DNA Is a Common Cause of Leigh’s Syndrome. Ann. Neurol. 1993;34:827–834. doi: 10.1002/ana.410340612. - DOI - PubMed
    1. Silva J.P., Köhler M., Graff C., Oldfors A., Magnuson M.A., Berggren P.-O., Larsson N.-G. Impaired Insulin Secretion and β-Cell Loss in Tissue-Specific Knockout Mice with Mitochondrial Diabetes. Nat. Genet. 2000;26:336–340. doi: 10.1038/81649. - DOI - PubMed

Publication types

Grants and funding

This work was supported by the Creative Challenge Program (2020R1|1A1A01060923) to Adhimoolam Karthikeyan (A.K.) and the Basic Science Research Program (2019R1A6A1A11052070 and 2022R1A2B5B02001711) to Taesun Min (T.M.) through the National Research Foundation of Korea (NRF), Ministry of Science and ICT.

LinkOut - more resources