Increased intramitochondrial free iron is a key feature of various liver diseases, leading to oxidative stress, mitochondrial dysfunction, and liver damage. Polydatin is a polyphenol with a hepatoprotective effect, which has been attributed to its ability to enhance mitochondrial oxidative metabolism and antioxidant defenses, thereby inhibiting reactive oxygen species (ROS) dependent cellular damage processes and liver diseases. However, it has not been explored whether polydatin is able to exert its effects by protecting the phospholipid cardiolipin against damage from excess iron. Cardiolipin maintains the integrity and function of electron transport chain (ETC) complexes and keeps cytochrome c bound to mitochondria, avoiding uncontrolled apoptosis. Therefore, the effect of polydatin on oxidative lipid damage, ETC activity, cytochrome levels, and ROS production was explored in iron-exposed rat liver mitochondria. Fe²⁺ increased lipid peroxidation, decreased cardiolipin and cytochromes c + c₁ and aa₃ levels, inhibited ETC complex activities, and dramatically increased ROS production. Preincubation with polydatin prevented all these effects to a variable degree. These results suggest that the hepatoprotective mechanism of polydatin involves the attenuation of free radical production by iron, which enhances cardiolipin levels by counteracting membrane lipid peroxidation. This prevents the loss of cytochromes, improves ETC function, and decreases mitochondrial ROS production.

Aging is a process characterized by tissue degeneration, increased susceptibility to chronic degenerative diseases, infections, and the appearance of neoplasms, which leads to disability and a reduction in the length and quality of life. This phenomenon is the result of the convergence of multiple processes, including mitochondrial dysfunction, fibrosis, inflammation, dysregulation of cell death processes, and immunosenescence. These processes have as their point of convergence an increase in the production of ROS. Avocado oil (Persea americana Mill.) contains a diverse array of bioactive compounds, including oleic acid, phytosterols, chlorophylls, xanthones, xanthines, and carotenoids. These bioactive compounds have the capacity to modulate the excessive production of ROS, thereby reducing the progression of age-related diseases and extending lifespan in experimental models of aging. In addition, several studies have demonstrated the efficacy of avocado oil in mitigating age-related diseases, including hypertension; insulin resistance; diabetes; non-alcoholic liver disease; and degenerative processes such as hearing loss, cognitive decline, neurodegeneration, and impaired wound healing. In light of these findings, it is hypothesized that avocado oil is a promising agent capable of promoting healthspan in later stages of life owing to its direct antioxidant actions and the activation of pathways that enhance endogenous antioxidant levels.

Obesity is a chronic disease that impairs skeletal muscle function, affects the ability to contract, and promotes the development of fatigue. For this reason, the study of treatments that seek to reduce the harmful effects of obesity on muscle tissue has been deepened. Diazoxide treatment and various exercise protocols have been proposed to protect skeletal muscle against oxidative stress and its effects. However, the intensity and duration of exercise combined with diazoxide that would obtain the best results for improving skeletal muscle function in obese rats is unknown. To this end, this study evaluated the effects of three different exercise intensities combined with diazoxide on contraction capacity, resistance to fatigue, markers of oxidative stress, lipid peroxidation, ROS, and glutathione redox status of skeletal muscle. The results showed that treatments with diazoxide and exercise at different intensities improved muscle contraction capacity by reducing oxidative stress during obesity, with the best results being obtained with low-intensity exercise in combination with diazoxide. Therefore, these results suggest that diazoxide and low-intensity exercise improve muscle function during obesity by decreasing oxidative stress with the same efficiency as a moderate-intensity exercise protocol.

Diabetes mellitus is a chronic degenerative disease characterized by hyperglycemia and oxidative stress. Iron catalyzes free radical overproduction. High iron concentrations have previously been reported to promote an increase in oxidative stress; however, the effect of iron restriction in diabetes has not yet been explored, so we tested to see if iron restriction in diabetic rats reduces oxidative damage and improved muscle function. Wistar rats were assigned to 4 groups: Control; Diabetic; Diabetic rats with a high iron diet, and Diabetic with dietary iron restriction. After 8 weeks the rats were sacrificed, the muscles were extracted to prepare homogenates, and serum was obtained for biochemical measurements. Low iron diabetic rats showed an increase in the development of muscle strength in both muscles. Dietary iron restriction decreased triglyceride concentrations compared to the untreated diabetic rats and the levels of extremely low-density lipoproteins. Aggravation of lipid peroxidation was observed in the diabetic group with a high iron diet, while these levels remained low with iron restriction. Iron restriction improved muscle strength development and reduced fatigue times; this was related to better lipid profile control and decreased oxidant stress markers.

High-fat and high-carbohydrate (HF-HC) diets induce metabolic syndrome via mitochondrial dysfunction and oxidative stress. We have previously shown that this may be prevented by avocado oil, a source of bioactive molecules with antioxidant properties. However, it is unknown if these effects are mediated by the unsaponifiable fraction of avocado oil (UFAO). Thus, we tested if this fraction improves glucose metabolism, bioenergetics and oxidative stress in mitochondria from the kidney and liver of rats fed an HF-HC diet. We found that 12 weeks of an HF-HC diet impaired glucose utilization and increased insulin resistance, which was prevented by UFAO administration. The HF-HC diet decreased respiration, membrane potential and electron transport chain (ETC) function in liver and kidney mitochondria. These mitochondrial dysfunctions were prevented by UFAO intake. Unexpectedly, UFAO increased ROS levels in the mitochondria of control animals and did not decrease them in rats with an HF-HC diet; however, UFAO protects liver and kidney mitochondria from iron-induced oxidative stress. These findings suggest that impairments in glucose metabolism and mitochondrial function by an HF-HC diet may be prevented by UFAO, without decreasing ROS generation but protecting mitochondria from oxidative damage.

En un mundo donde las enfermedades crónicas como la diabetes, la hipertensión y el hígado graso son cada vez más comunes, la importancia de una alimentación balanceada se vuelve esencial. Aunque parezca sencillo, llevar una dieta equilibrada es un desafío diario, complicado por la falta de tiempo y una desinformación general sobre los alimentos benéficos para nuestra salud. Aquí es donde entra en juego un superalimento poco reconocido: el aceite de aguacate. Este verdadero “oro verde” ha capturado la atención de la comunidad científica debido a sus notables beneficios. Con un alto contenido en grasas benéficas para la salud, vitaminas y antioxidantes, el aceite de aguacate no solo es un aliado en la cocina, sino también en nuestra lucha contra las enfermedades crónicas. Este artículo explora cómo el aceite de aguacate puede ser un componente clave en nuestra dieta diaria, ofreciendo una solución natural y accesible para mejorar nuestra salud y disminuir la severidad de las complicaciones de enfermedades crónicas a largo plazo. Acompáñanos en este viaje para descubrir los secretos del aceite de aguacate y cómo puede ayudarnos a llevar una vida más sana.