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Acne vulgaris is a chronic inflammatory skin disease of the pilosebaceous unit. Its pathogenesis is multifactorial and involves the overlap between four main processes: alteration of the keratinization, increased sebum production, colonization with Cutibacterium acnes, and inflammation. The role of oxidative stress (OS) has been intensively studied in inflammatory skin conditions such as psoriasis, vitiligo, or atopic dermatitis. However, the involvement of OS in the pathogenesis of acne is less known. The evidence accumulated over the last decade suggests that in the case of acne patients, there is an imbalance between oxidants and antioxidants. In this review, we analyzed studies that evaluated markers of OS in patients with acne, published in the last ten years, with the aim of providing new insights into the pathogenesis of acne. [ABSTRACT FROM AUTHOR]

Recent research has highlighted the role of oxidative stress in the pathogenesis of HPV-related lesions, especially in neoplastic diseases. Oxidative stress and chronic inflammation are the most important cofactors that HPV requires to persist and induce a malignant process. Data on the role of oxidative stress in benign lesions associated with HPV infection, such as genital and non-genital warts, is scarce and further research is needed. We have determined markers of oxidative stress in the serum of 26 patients with palmoplantar warts and 28 healthy subjects. We have investigated representative markers for the four main molecular targets of oxidative stress, nucleic acids - 8-hydroxy-2'-deoxyguanosine (8-OHdG), lipids - 4-hydroxynonenal (4-HNE), carbohydrates - pentosidine, and proteins - thiol-disulfide homeostasis parameters (TDHP): total thiol (TT), native thiol (NT), and disulfides (DS). The serum levels of oxidative stress markers, 4-HNE, 8-OHdG, and pentosidine, were statistically significantly higher in patients with warts in comparison to the control group (p < 0.01). Regarding TDHP, we have found that TT levels were statistically significantly higher in the patient group compared to the control one (p < 0.05). Even though NT and DS levels were reported to be higher in the patient group compared to the control one, no statistical significance was established (p > 0.05). Our results show enhanced oxidative stress damage in patients with palmoplantar warts and provide valuable data in understanding the molecular mechanisms involved in the pathogenesis of HPV infection. To the best of our knowledge, this is the first study to evaluate both 4-HNE and pentosidine in patients with palmoplantar warts. [ABSTRACT FROM AUTHOR]

Human papillomavirus (HPV) is a small double-stranded DNA virus with tropism for epithelial cells. To this date, over 150 genotypes are known and are classified into two major groups, low-risk and high-risk strains, depending on the ability of the virus to induce malignant transformation. The host's immunity plays a central role in the course of the infection; therefore, it may not be clinically manifest or may produce various benign or malignant lesions. The pathogenic mechanisms are complex and incompletely elucidated. Recent research suggests the role of chronic inflammation and oxidative stress (OS) in the pathogenesis of HPV infection and the associated carcinogenic processes. Chronic inflammation induces OS, which in turn promotes the perpetuation of the inflammatory process resulting in the release of numerous molecules which cause cell damage. Reactive oxygen species exert a harmful effect on proteins, lipids, and nucleic acids. Viral oncogenes E5, E6, and E7 are involved in the development of chronic inflammation through various mechanisms. In addition, HPV may interfere with redox homeostasis of host cells, inducing OS which may be involved in the persistence of the infection and play a certain role in viral integration and promotion of carcinogenesis. Knowledge regarding the interplay between chronic inflammation and OS in the pathogenesis of HPV infection and HPV-induced carcinogenesis has important consequences on the development of new therapeutic strategies. [ABSTRACT FROM AUTHOR]

Significant progress has been made in the therapy of hepatitis C, but many things are still unknown about its pathogenesis. The course of hepatitis C is influenced by both host and virus characteristics. More and more studies highlight the role of oxidative stress in the pathogenesis of hepatitis C. Core protein plays a key role in the generation of reactive oxygen species. In addition, the most important complications of the infection, cirrhosis and hepatocellular carcinoma, seem to be related to the presence of oxidative stress. In this context antioxidants could be a useful adjuvant therapy. [ABSTRACT FROM AUTHOR]