Oxidative stress (OS) has greatly interested the research community in understanding damaging processes occurring in cells. OS is triggered by an imbalance between reactive oxygen species (ROS) production and their elimination by the antioxidant system; however, ROS function as second messengers under physiological conditions. ROS are produced from endogenous and exogenous sources. Endogenous sources involve mitochondria, nicotinamide adenine dinucleotide phosphate hydrogen (NADPH), oxidases (NOXs), endoplasmic reticulum (ER), xanthine oxidases (XO), endothelial nitric oxide synthase (eNOs), and others. In contrast, exogenous ROS might be generated through ultraviolet (UV) light, ionizing radiation (IR), contaminants, and heavy metals, among others. It can damage DNA, lipids, and proteins if OS is not controlled. To avoid oxidative damage, antioxidant systems are activated. In the present review, we focus on the basic concepts of OS, highlighting the production of reactive oxygen and nitrogen species (RONS) derived from internal and external sources and the last elimination. Moreover, we include the cellular antioxidant system regulation and their ability to decrease OS. External antioxidants are also proposed as alternatives to ameliorate OS. Finally, we review diseases involving OS and their mechanisms.

Severe acute respiratory syndrome coronavirus type 2 (SARS‐CoV‐2) causes coronavirus disease 2019 (COVID‐19), characterised by high levels of inflammation and oxidative stress (OS). Oxidative stress induces oxidative damage to lipids, proteins, and DNA, causing tissue damage. Both inflammation and OS contribute to multi‐organ failure in severe cases. Magnesium (Mg 2+ ) regulates many processes, including antioxidant and anti‐inflammatory responses, as well as the proper functioning of other micronutrients such as vitamin D. In addition, Mg 2+ participates as a second signalling messenger in the activation of T cells. Therefore, Mg 2+ deficiency can cause immunodeficiency, exaggerated acute inflammatory response, decreased antioxidant response, and OS. Supplementation with Mg 2+ has an anti‐inflammatory response by reducing the levels of nuclear factor kappa B (NF‐κB), interleukin (IL) ‐6, and tumor necrosis factor alpha. Furthermore, Mg 2+ supplementation improves mitochondrial function and increases the antioxidant glutathione (GSH) content, reducing OS. Therefore, Mg 2+ supplementation is a potential way to reduce inflammation and OS, strengthening the immune system to manage COVID‐19. This narrative review will address Mg 2+ deficiency associated with a worse disease prognosis, Mg 2+ supplementation as a potent antioxidant and anti‐inflammatory therapy during and after COVID‐19 disease, and suggest that randomised controlled trials are indicated.

Oxidative stress (OS) represents one of the main mechanisms of toxicity induced by environmental pollutants such as cadmium (Cd). OS is a natural physiological process where the presence of oxidants, such as reactive oxygen-derived species (ROS), outweighs the strategy of antioxidant defenses, culminating in the interruption of signaling and redox control. It has been suggested that Cd increases ROS mainly by inducing damage to the electron transport chain and by increasing the activity of nicotinamide adenine dinucleotide hydrogen phosphate (NADPH) oxidase (NOX) and the concentration of free iron (Fe), as well as causing a decrease in antioxidant defense. On the other hand, OS has been related to changes in the biology of the epigenome, causing adverse health effects. Recent studies show that Cd generates alterations in deoxyribonucleic acid (DNA) methylation, histone modifications, and noncoding RNA (ncRNA) expression. However, the role of OS in Cd-induced epigenetic modifications is still poorly explored. Therefore, this review provides an update on the basic concepts of OS and its relationship with Cd-induced epigenetic changes. Furthermore, the use of antioxidant compounds is proposed to mitigate Cd-induced epigenetic alterations.

Magnesium (Mg2+) is an essential mineral nutrient, necessary for many biochemical reactions in the human body, including energy metabolism, protein and DNA synthesis, maintenance of the electrical potential of nervous and cardiac tissues, control of blood glucose, and regulation of blood pressure. However, currently, the world population suffers from a severe problem because the consumption of Mg2+ in the diet is deficient and generalized in the populations. Mg2+ deficiency causes oxidative stress (OS) due to the increase in reactive oxygen species (ROS) that originate from mitochondrial dysfunction, activation of the renin-angiotensin-aldosterone system (RAAS), and abnormal regulation of calcium homeostasis. In addition, Mg2+ deficiency also causes inflammation by increasing the production of proinflammatory molecules such as interleukin (IL)-1, IL-6, and tumor necrosis factor-alpha (TNF-α), which in turn can exacerbate the production of ROS. The combination of inflammation and OS induced by Mg2+ deficiency increases the risk of developing chronic diseases. This review describes Mg2+ deficiency, its complications, and its relationship with OS and chronic inflammatory diseases. In addition, the importance of increasing the intake of Mg2+ throughout the world is highlighted.

Aerobic living systems use oxygen (O2) for energy production. However, O2 can become toxic due to the production of reactive oxygen species (ROS). ROS have complex cell signaling functions, but under an uncontrolled increase in their production, oxidative stress (OS) results, which can cause damage to cellular structures (lipids, proteins, nucleic acids). Faced with an oxidative attack, the cell must establish a rapid and efficient antioxidant response to prevent or remove damage to a target molecule. Thus, cells possess an antioxidant system that allows them to modulate ROS levels and achieve redox homeostasis. This article reviews and discusses the basic concepts regarding ROS and antioxidant defenses.