ABSTRACT
Pomegranate (Punica granatum) is valued for its health-promoting properties, largely due to its rich phenolic content, including flavonoids, tannins, and phenolic acids. These bioactive compounds, especially abundant in the peel and seeds, exhibit strong antioxidant, antidiabetic, and cytotoxic activities. Up to 35 phenolic compounds have been identified, with gallic acid, ellagic acid, and punicalagin showing significant biological effects. The antioxidant potential of pomegranate is linked to its ability to combat oxidative stress and reduce risks of chronic diseases like diabetes and cardiovascular conditions. Its antidiabetic activity involves mechanisms such as Nrf2 pathway activation, improving antioxidant defense and metabolic profiles. Additionally, certain compounds, notably punicalagin, demonstrate cytotoxicity against cancer cell lines, indicating potential in cancer therapy. However, variations in phenolic content due to cultivar differences and extraction techniques pose challenges in standardizing its use. Ongoing research aims to elucidate the underlying mechanisms and support therapeutic applications of pomegranate.
References
- [1] Armstrong BK, Kricker A. The epidemiology of UV-induced skin cancer. Photochem Photobiol Sci. 2001;116(84447):Persuasive evidence that each of the three main skin cancers.
- [2] Cadet J, Douki T. Formation of UV‑induced DNA lesions: cyclobutane pyrimidine dimers and 6–4 photoproducts. Photochem Photobiol Sci. 2018;17(12):1816–35.
- [3] Mouret S, Baudouin C, Charveron M, Favier A, Cadet J, Douki T. Cyclobutane pyrimidine dimers predominate in human skin exposed to UVA. Proc Natl Acad Sci U S A. 2006;103(37):13765–70.
- [4] Fan F, et al. Mechanism of ultraviolet radiation‑induced basal cell carcinoma. Ann Transl Med. 2023;11(55995).
- [5] Mouret S, et al. Cooperation between base and nucleotide excision repair on UV lesions. Genet Mol Biol (São Paulo). 2006;29(4):some pages.
- [6] Paulo MS, Symanzik C, Ádam B, et al. Risk of cutaneous squamous cell carcinoma due to occupational solar ultraviolet exposure: protocol. PLoS One. 2023;18(3):e0282664.
- [7] Gobba F, Modenese A, John SM. Skin cancer in outdoor workers exposed to solar radiation in Italy. J Eur Acad Dermatol Venereol. 2019;33:2068–2074.
- [8] Ling G, Persson A, et al. Persistent p53 mutations in single cells from normal skin. Am J Pathol. 2001;159(4):1247–54.
- [9] Glass AG, Hoover RN. The rising epidemic of melanoma and non‑melanoma skin cancers. Photochem Photobiol. 1989;38(5):569–75.
- Bajdik CD, Gallagher RP, Astrakianakis G, et al. Non‑solar UV radiation and risk of basal and squamous cell cancer. Br J Cancer. 1996;73(11):1612–4.
- de Winter S, et al. Solar‑simulated UV exposure and epidermal DNA damage. J Invest Dermatol. 2001;117(4):867–74.
- Cadet J, Anselmino C, Douki T, Voituriez L. Photochemistry of nucleic acids in cells: UV‑induced DNA damage. Photochem Photobiol Sci.
- Beani JC. Ultraviolet A‑induced DNA damage: role in skin cancer. Bull Acad Natl Med. 2014;198(2):273–95.
- Anderson MW, Hewitt JP, Spruce SR. Broad spectrum physical sunscreens: TiO₂ and ZnO. Photodermatol Photoimmunol Photomed.
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