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Approximately 5-20% of HNSCC patients experience second primary cancers within the first 5 years of treatment, contributing to high mortality rates. Epidemiological evidence has linked a low dietary intake of antioxidants to an increased risk of cancer, especially squamous cell carcinoma, prompting research into their potential in neoplasm chemoprevention. Cigarette smoking is the primary risk factor for HNSCC, and a diet rich in antioxidants offers protective effects against head and neck cancer. Paradoxically, smokers, who are at the highest risk, tend to consume fewer antioxidant-rich fruits and vegetables. This has led to the hypothesis that integrating antioxidants into the diet could play a role in both primary and secondary prevention for at-risk individuals. Furthermore, some HNSCC patients use antioxidant supplements during chemotherapy or radiotherapy to manage side effects, but their impact on cancer outcomes remains uncertain. This systematic review explores the evidence for the potential use of antioxidants in preventing second primary cancers in HNSCC patients. In conclusion, none of the antioxidants tested so far (α-tocopherol, β-carotene, JP, Isotretinoin, interferon α-2a, vitamin E, retinyl palmitate, N-acetylcysteine) was effective in preventing second primary tumors in HNSCC patients, and they could only be used in reducing the side effects of radiotherapy. Further research is needed to better understand the interplay between antioxidants and cancer outcomes in this context.

Introduction: OSAS is a disease that affects 2% of men and 4% of women of middle age. It is a major health public problem because untreated OSAS could lead to cardiovascular, metabolic, and cerebrovascular complications. The more accepted theory relates to oxidative stress due to intermittent hypoxia, which leads, after an intense inflammatory response through multiple pathways, to endothelial damage. The objective of this study is to demonstrate a correlation between OSAS and hearing loss, the effect of the CPAP on hearing function, and if oxidative stress is also involved in the damaging of the hearing system., Methods: A review of the literature has been executed. Eight articles have been found, where seven were about the correlation between OSAS and the hearing system, and only one was about the CPAP effects. It is noted that two of the eight articles explored the theory of oxidative stress due to intermittent hypoxia., Results: All studies showed a significant correlation between OSAS and hearing function ( p < 0.05)., Conclusions: Untreated OSAS affects the hearing system at multiple levels. Oxidative stress due to intermittent hypoxia is the main pathogenetic mechanism of damage. CPAP has no effects (positive or negative) on hearing function. More studies are needed, with the evaluation of extended high frequencies, the execution of vocal audiometry in noisy environments, and the evaluation of potential biomarkers due to oxidative stress.

Alcohol consumption is associated with oxidative stress and an increased risk of carcinoma of the upper aero-digestive tract (UADT). Recently, it has been found that some microorganisms in the human oral cavity may locally metabolize ethanol, forming acetaldehyde, a carcinogenic metabolite of alcohol. In a cohort of patients first visited for UADT cancers, we estimated their alcohol consumption by measuring Ethyl Glucuronide/EtG (a long-lasting metabolite of ethanol) in the hair and carbohydrate-deficient transferrin/CDT (short-term index of alcohol intake) in the serum. Moreover, we analyzed, by culture-based methods, the presence of Neisseria subflava , Streptococcus mitis , Candida albicans , and glabrata (microorganisms generating acetaldehyde) in the oral cavity. According to the EtG values, we correlated drinking alcohol with endogenous oxidative stress and the investigated microorganism's presence. We found that 55% of heavy drinkers presented microorganisms generating acetaldehyde locally. Moreover, we found that the presence of oral acetaldehyde-producing bacteria correlates with increased oxidative stress compared to patients without such bacteria. As for the study of alcohol dehydrogenase gene polymorphisms (the enzyme that transforms alcohol to acetaldehyde), we found that only the "CGTCGTCCC" haplotype was more frequent in the general population than in carcinoma patients. This pilot study suggests the importance of estimating alcohol consumption (EtG), the presence of bacteria producing acetaldehyde, and oxidative stress as risk factors for the onset of oral carcinomas.

Oxidative stress is a condition determined by an imbalance between antioxidant and oxidative factors. Oxidative stress can have serious consequences on our organism. Indeed, it causes both necrosis and cell apoptosis, determining cellular aging, increased carcinogenesis, vascular stiffening, increased autoimmune diseases, and muscle decay. In the context of pediatric syndromes, oxidative stress could play a role in the first order. In fact, our review of the literature showed that in some pathologies, such as fetal alcohol spectrum disorders, oxidative stress related to the intake of ethanol during pregnancy is a main etiological factor determining the associated clinical syndrome. On the contrary, in Williams syndrome, Down syndrome, Marfan syndrome, Gaucher syndrome, ataxia-telangiectasia, autistic spectrum disorder, Fanconi's anemia, and primitive immunodeficiencies, the increase in oxidative stress is directly associated with the genetic alterations that cause the same pathologies. Although further studies are needed to better understand the relationship between oxidative stress and pediatric diseases, a better knowledge of this crucial issue encourages future therapeutic strategies.

Head and neck cancer (HNC) concerns more than 890,000 patients worldwide annually and is associated with the advanced stage at presentation and heavy outcomes. Alcohol drinking, together with tobacco smoking, and human papillomavirus infection are the main recognized risk factors. The tumorigenesis of HNC represents an intricate sequential process that implicates a gradual acquisition of genetic and epigenetics alterations targeting crucial pathways regulating cell growth, motility, and stromal interactions. Tumor microenvironment and growth factors also play a major role in HNC. Alcohol toxicity is caused both directly by ethanol and indirectly by its metabolic products, with the involvement of the oral microbiota and oxidative stress; alcohol might enhance the exposure of epithelial cells to carcinogens, causing epigenetic modifications, DNA damage, and inaccurate DNA repair with the formation of DNA adducts. Long-term markers of alcohol consumption, especially those detected in the hair, may provide crucial information on the real alcohol drinking of HNC patients. Strategies for prevention could include food supplements as polyphenols, and alkylating drugs as therapy that play a key role in HNC management. Indeed, polyphenols throughout their antioxidant and anti-inflammatory actions may counteract or limit the toxic effect of alcohol whereas alkylating agents inhibiting cancer cells' growth could reduce the carcinogenic damage induced by alcohol. Despite the established association between alcohol and HNC, a concerning pattern of alcohol consumption in survivors of HNC has been shown. It is of primary importance to increase the awareness of cancer risks associated with alcohol consumption, both in oncologic patients and the general population, to provide advice for reducing HNC prevalence and complications.