Oxidative damage and antioxidants in cervical cancer

Abstract

The pathogenesis of cervical cancer is related to oxidative damage caused by persistent infection by one of the oncogenic types of human papillomavirus (HPV). This damage comes from oxidative stress, which is the imbalance caused by the increase in reactive oxygen and nitrogen species and impaired antioxidant mechanisms, promoting tumor progression through metabolic processes. The incorporation of HPV into the cellular genome leads to the expression of oncoproteins, which are associated with chronic inflammation and increased production of reactive oxygen species, oxidizing proteins, lipids and DNA. The increase in these parameters is related, in general, to the reduction of circulating levels of enzymatic antioxidants—superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase; and non-enzymatic antioxidants—reduced glutathione, coenzyme Q10 and vitamins A, C and E, according to tumor staging. In contrast, some enzymatic antioxidants suffer upregulation in the tumor tissue as a way of adapting to the oxidative environment generated by themselves, such as glutathione-S-transferase, reduced glutathione, glutathione peroxidase, superoxide dismutase 2, induced nitric oxide synthase, peroxiredoxins 1, 3 and 6, and thioredoxin reductase 2. The decrease in the expression and activity of certain circulatory antioxidants and increasing the redox status of the tumor cells are thus key to cervical carcinoma prognosis. In addition, vitamin deficit is considered a possible modifiable risk factor by supplementation, since the cellular functions can have a protective effect on the development of cervical cancer. In this review, we will discuss the impact of oxidative damage on cervical cancer progression, as well as the main oxidative markers and therapeutic potentialities of antioxidants.

To Be or Not to Be? Are Reactive Oxygen Species, Antioxidants, and Stress Signalling Universal Determinants of Life or Death?

“…The imbalances in peroxisomal H 2 O 2 metabolism have been associated with multiple oxidative stress-related human and animals disease states, and it can be linked to alterations in CAT activity [ 93 , 162 , 163 , 164 , 165 , 166 , 167 , 168 ]. CAT modulates the expression of numerous genes, i.e., CAT inhibition or overexpression can activate or inhibit the activity of NF-κB.…”

Therapeutic Effects of Natural Products on Cervical Cancer: Based on Inflammatory Pathways

“…The chances of cancer cells appearing in this imbalance are greatly increased. Oncogene E6 activates glutathione (GSH) and catalase (CAT), so the appearance of damage and mutation of normal cellular DNA becomes reasonable (Hemmat and Bannazadeh Baghi, 2019;Preci et al, 2021). Notably, nitric oxide (NO) also induces transcription of oncogenes E6 and E7, suggesting a mutually reinforcing mechanism between HPV infection, inflammatory response and oxygen nitration response (Bogdan, 2001).…”

A Narrative Review of the Role of Diet and Lifestyle Factors in the Development and Prevention of Endometrial Cancer

“…For example, Korean women who consumed higher amounts of gamma-tocopherol showed a 72% lower risk of developing ovarian cancer compared to women who have not [ 239 ]. Although the effect of vitamin E and other anti-oxidant vitamins on the prevention of DNA damage is modest [ 240 ], they do have a contributory role in cancer prevention [ 241 , 242 , 243 ] that is starting to be exploited therapeutically [ 244 ].…”