The fine regulation of antioxidant systems and intracellular production of reactive oxygen species (ROS) is responsible for cellular redox balance. The main organelles responsible for ROS production are mitochondria, and they complete this process through the electron transport chain. These potentially harmful molecules are buffered by enzymatic and non-enzymatic antioxidant systems. Oxidative stress is determined by an imbalance between the production and clearance of ROS in favor of the accumulation of these detrimental species, which generate cellular damage by interacting with macromolecules. In neurodegenerative diseases, oxidative stress has been demonstrated to be a crucial component, both causal and consequential to the disease itself. On the other hand, neurodegeneration disrupts neuromuscular junctions, leading to reduced muscle use and subsequent atrophy. Additionally, systemic inflammation and metabolic dysfunction associated with neurodegenerative diseases exacerbate muscle degeneration. Thus, sarcopenia and atrophy are common consequences of neurodegeneration and play a significant role in these disorders. Regarding this, ROS have been defined as promoting sarcopenia, stimulating the expression of genes typical of this condition. Overall, this review aims to contribute to filling the gap in the literature regarding the consequences at the muscular level of the relationship between oxidative stress and neurodegenerative diseases.

Background/Objectives: Colorectal cancer (CRC) is one of the most aggressive malignancies and has a very high mortality rate. Several studies have shown that obesity and hyperlipidemia are among the factors implicated in the onset of this disease. These factors can be modified through lifestyle changes, and diet plays a crucial role in this context. We evaluated the effects of Tuber borchii (T. borchii) fungal extracts based on experimental evidence showing that some truffles produce antioxidant, anti-inflammatory, and anticancer secondary metabolites. Methods: To this end, we treated human colorectal cancer cells (HCT 116) with various extracts of T. borchii at different time points and concentrations. Results and Conclusions: The results showed that the treatments caused a decrease in cell proliferation due to the induction of apoptotic cell death, as evidenced by FACS analyses. The apoptotic pathway was confirmed by the increase in the cleavage of Caspase 3 and Caspase 9. We then investigated the molecular mechanisms underlying cell death, finding increased nuclear localization of p53 and increased expression of its downstream pro-apoptotic genes, PUMA and NOXA. Among the upstream signaling events, we identify an increase in p-ERK1/2, a MAPK member involved in several antiproliferative/pro-apoptotic insults.