No abstract

Recent studies have addressed the possibility of an association between polycystic ovaries and ovarian cancer. DNA damage is the first step of the carcinogenesis, and susceptibility to cancer, in general, is characterized by high DNA damage. Free radical-mediated DNA damage and impaired antioxidant defence have been implicated as contributory factors for the development of cancer. This study evaluates DNA damage (strand breakage, base oxidation, formamidopyrimidine DNA glycosylase (Fpg) sensitive sites), H2O2-induced DNA damage, a marker of DNA susceptibility to oxidation and glutathione (GSH) level, a powerful antioxidant, in women with polycystic ovary syndrome (PCOS). Women with PCOS showed a significant decrease in GSH level, a significant increase in DNA strand breakage and H2O2-induced DNA damage. Although Fpg-sensitive sites were higher in the PCOS group compared to the control group, the difference did not reach a statistically significant level. Significant correlations were found between free testosterone and DNA strand breakage (r = 0.46, p<0.01) and free testosterone and H2O2-induced DNA damage (r = 0.41, p<0.05). The data indicate that DNA damage and susceptibility of DNA to oxidative stress are increased in women with PCOS and may explain the association between PCOS and ovarian cancer.

Huntington's disease (HD) is a neurodegenerative disorder characterized by progressive loss of neurons, which leads to behavioral systems and mental decline. HD is linked to repeat expansions of cytosine, adenine, and guanine in the Huntingtin (HTT) gene that give rise to mutation, leading to the formation of the HTT protein product. Oxidative stress also provokes the initiation and progression of HD as it leads to protein misfolding that results in the formation of inclusion which clumps together and alters neurotransmission. Despite the advancement in the field of pharmaceutical sciences, current therapeutic approaches suppress only the severity of symptoms and no therapy exists that can cure HD from its root cause. Flavonoids are the most abundant polyphenols widely present in daily dietary sources. Dietary flavonoids have a wide range of pharmacological bioactivities and many therapeutic applications. Dietary flavonoids including hesperidin, naringin, quercetin, rutin, fisetin, myricetin, luteolin, and epigallocatechin 3-O-gallate can prevent and manage HD through exerting antioxidant and anti-inflammatory activities, altering intracellular pathways, genetic alterations, and metal ion chelation. This review highlights flavonoids as therapeutic options for HD and will open new dimensions for flavonoids as safe and effective therapeutic agents in diminishing HD.

In recent years much attention has been focused on the role of glutathione (GSH) and GSH-related enzymes such as glutathione peroxidase (GSH Px), glutathione reductase (GSH Red), and glutathione S-transferase (GST) in the inhibition of free radical-induced carcinogenesis. In this study, erythrocyte GSH levels and activities of GSH Px, GSH Red, and GST were determined in patients with colorectal tumors (n = 20, mean age 54.5 +/- 8.3 yr). Erythrocyte GSH Red and GST activities were significantly higher in patients with colorectal tumors. Erythrocyte GSH levels and GSH Px activities were found to be significantly decreased in the patients. When the patients were classified based on their clinical grading (Dukes classifications), there was no significant difference in studied parameters between Dukes B and Dukes C. Our results suggest that oxidative stress may play an important role in colorectal tumorigenesis and that these events have no effect on the clinical grading of the colorectal tumor.