RESUMO
Ferroptosis is a recently identified form of cell death characterized by iron accumulation and lipid peroxidation. Unlike apoptosis, necrosis, and autophagy, ferroptosis operates through a distinct molecular pathway. Curcumin, derived from turmeric rhizomes, is a natural compound with diverse therapeutic benefits, including neuroprotective, anti-metabolic syndrome, anti-inflammatory, and anti-cancer properties. Growing evidence suggests that curcumin possesses both pro-oxidant and antioxidant properties, which can vary depending on the cell type. In this review, we explore the relationship between the effects of curcumin and the molecular mechanisms underlying the ferroptosis signaling pathway, drawing from current in vivo and in vitro research. Curcumin has been found to induce ferroptosis in cancer cells while acting as an inhibitor of ferroptosis in tissue injuries. Notably, curcumin treatment leads to alterations in key ferroptosis markers, underscoring its significant impact on this process. Nonetheless, further research focused on elucidating this important attribute of turmeric is crucial for advancing disease treatment.
RESUMO
Oxidative stress maybe involved in the patho-etiology of menstrual-associated complications. Curcuminoids, are polyphenolic natural compounds that have potentially important functional activities. This triple-blind, randomized, placebo-controlled trial was performed to investigate the effects of a curcuminoids on oxidative stress and antioxidant capacity in girls with premenstrual syndrome (PMS) and dysmenorrhea. Eighty young girls with both PMS and dysmenorrhea were randomly given either curcuminoids (500 mg+5 mg piperine) or a placebo daily, for a period from 7 days pre- until 3 days post- initiation of menstrual bleeding for 3 successive menstrual cycles. The total antioxidant capacity and free radical scavenging activity of serum and urine were quantified via ferric reducing/antioxidant power (FRAP) and 1,1-diphenyl-2-picrylhydrazyl (DPPH) methods, respectively. There were no significant differences between the placebo and curcumin groups, with respect to the age, dietary intake and biochemical/anthropometric indices (p>0.05). The curcumin treatment significantly increased the free-radical scavenging activity of serum compared to the treatment with placebo (p=0.031). Although, no significant changes were found in serum and urinary levels of FRAP, DPPH and MDA between the groups (p>0.05). Curcumin treatment did increase free-radical scavenging activity and antioxidant potential in girls with PMS and dysmenorrhea. Investigations with higher doses and duration of curcumin are required to verify our findings.
RESUMO
One of the newly recognized types of cell death is ferroptosis which is related to the accumulation of iron and lipid-reactive oxygen species. Ferroptosis is considered a programmed cell death with a different mechanism from apoptosis, necrosis, and autophagy. Emerging evidence suggests that ferroptosis may occur in the context of cardiovascular disease (CVD), cancer, neurodegenerative diseases, and non-alcoholic fatty liver disease (NAFLD). Statins are the first-line therapy for dyslipidemia. The suppression of the HMG-CoA reductase by statins leads to decreased expression of glutathione peroxidase 4 (GPX4), a key regulator of lipid peroxidation, which in turn results in lipid ROS production and induction of ferroptosis. Experimental data suggest that statins may act as anti-cancer drugs by enhancing tumor cells' ferroptosis. In contrast, statins have also been reported to mitigate ferroptosis in animal models of myocardial ischemia-reperfusion and heart failure. This mini-review presents statin effects on the ferroptosis pathway, based on up-to-date in vivo and in vitro research. Furthermore, the potential impact of these effects on cardiometabolic diseases (e.g., CVD and NAFLD) and cancer is briefly discussed. Overall, there is a need for future studies focusing on statin-induced changes in ferroptosis as a therapeutic approach to such diseases.