The Preventive Effect of Dietary Antioxidants against Cervical Cancer versus the Promotive Effect of Tobacco Smoking

Abstract

Uterine cervical cancer is the fourth most common cancer in women, and its etiology has been recognized. High-risk human papilloma virus (HR-HPV) infection induces an opportunity for malignant transformation. This paper discusses the current issues based on a review of the literature and compares the impact of the dietary and nutrient intake to the impact of tobacco smoking on cervical cancer development. The important roles of diet/nutrition in cervical cancer are as prophylaxis against HR-HPV infection. Antioxidant vitamins can inhibit the proliferation of cancer cells, stabilize the p53 protein, prevent DNA damage, and reduce immunosuppression. In contrast, tobacco smoking not only causes DNA adducts and strand breaks, but it independently causes an increased viral load in HR-HPV-infected cells. Tobacco smoking induces the heightened expression of E6 and E7 and can inhibit the immune system response to HPV. What happens when two materials, which have opposite effects on cervical cells, are taken in at the same time? The negative effects of tobacco smoking may be stronger than the positive effects of vitamins, vegetables, and fruits on the regression of cervical disease such as cervical intraepithelial neoplasia (CIN). A relatively low intake of vitamins, vegetables, and fruits in combination with tobacco smoking was most associated with a high incidence of cervical neoplasia.

Effect of Alpha-Lipoic Acid Supplementation on Low-Grade Squamous Intraepithelial Lesions—Double-Blind, Randomized, Placebo-Controlled Trial

“…In the etiology of the formation of squamous intraepithelial lesions (SIL), HPV infection leads to the release of different inflammation mediators, resulting in the formation of reactive oxygen species (ROS) and causing a decrease in the level of antioxidants. HPV integration in combination with oxidative stress causes oxidative damage to the genome and different epigenetic alterations that altogether hinder apoptosis and alter cellular proliferation [ 3 ]. Therefore, diet components exerting antiviral, anti-inflammatory and antioxidant actions could be considered protective against the progression of SIL and the development of cervical cancer.…”

“…Observational studies confirm that Western dietary patterns increase the possibility of HPV infection, while high adherence to the Mediterranean diet decreases the risk [ 4 ]. Numerous observational studies indicate that the consumption of a wide variety of whole foods rich in vitamins, minerals and nonessential bioactive compounds (especially those with antioxidant and antiviral properties) can be effective in preventing the progression of LSILs to HSIL or cervical cancer, and, therefore, a balanced-diet prevention strategy should be recommended to patients upon LSIL diagnosis [ 3 , 5 , 6 , 7 ].…”

The Preventive Effect of Dietary Antioxidants on Cervical Cancer Development

“…Accelerators, in contrast, include environmental, immunological, and lifestyle cofactors such as cigarette smoking, diet, oral contraceptive (OC) use, parity, and coinfection with other sexually transmitted infections [ 10 ]. Indeed, we previously reviewed the effect of cigarette smoking on the risk of cervical cancer development [ 71 , 72 ], hypothesizing that the promotive effect of smoking may be stronger than the preventive effect of antioxidant intake against cervical cancer. Wei et al suggested that in HR-HPV-infected cells, tobacco smoking not only causes DNA adducts and strand breaks [ 73 ], but also causes an increase in the viral load [ 74 ].…”

A study on the correlation between the prognosis of HPV infection and lesion recurrence after cervical conization

“…Smoking has been shown to be an independent risk factor for HSIL in young women after the onset of frequent sexual activity (Collins et al, 2010). Several studies have shown (International Collaboration of Epidemiological Studies of Cervical Cancer et al, 2006;Koshiyama et al, 2019) that smokers have an increased risk of developing cervical cancer compared with nonsmokers, and that the risk of squamous cell carcinoma of smokers increases with the number of cigarettes smoked every day and with decreasing age of smoking initiation. Inamine et al (2012) found that smoking induces high plasma expression of vascular endothelial growth factor C (VEGF-C) in patients with CIN and that VEGF-C plays a major role in cervical lesions in smoking patients.…”