An Explicative Review on Nanotechnology-based Drug Delivery Systems for Alleviating Oxidative Stress-driven Pathologies.

Catalase overexpression attenuates angiotensinogen expression and apoptosis in diabetic mice

This review so far has considered the role of vascular cells in the generation of reactive oxygen species (ROS) and novel approaches to their detection in integrated systems such as animal models of vascular disease and humans. We now turn attention to evidence consistent with a role for ROS in models of human disease and in discrete patient populations. We also briefly comment on the outcomes of clinical trials of antioxidants. Mainly, these have been disappointing. However, it is premature to conclude that the oxidation hypothesis of disease causality has been adequately tested. Animal studies, for the most part, support a fundamental role for ROS in cardiovascular disease. Any controversy could in part reflect the use of ineffective antioxidants and the selection of models in which ROS generation is of marginal relevance to the measured outcome. Both of these issues require a quantitatively accurate measurement of drug effect (ie, antioxidant capacity) before hypotheses relating to the role of oxidant stress can be addressed rationally. These issues pertain to clinical trials also, as we will discuss. However, animal studies permit administration of much more powerful antioxidants (eg, rate constant for interaction of superoxide dismutase (SOD) with O2·− ≈1.6×109 · mol/L−1 · s−1) than is possible in humans (eg, rate constant for vitamin E ≈0.59 mol/L−1 · s−1) or, like in the case of vitamin E, doses of the antioxidant in excess of those usually applied in clinical research. ### Atherosclerosis Animal models of atherosclerosis have documented that all the constituents of the plaque produce and use ROS. Lesion formation is associated with the accumulation of lipid peroxidation products1,2 and induction of inflammatory genes,3 inactivation of NO·resulting in endothelial dysfunction, 4,5 activation of matrix metalloproteinases,6 and increased smooth muscle cell growth.7 …

In the scientific literature, there are no complete scientifically substantiated conclusion about the functional state of the antioxidant status of the skin, its scars and the possibilities of their local correction as part of complex therapy. We have analyzed the literature data reflecting the issues of complex therapy of cicatricial changes in the skin in order to determine the feasibility for the effective use of antioxidants in the local correction of oxidative stress disorders. The pathophysiological aspects of free radical mechanisms of skin scar formation have been studied. The cell pool that forms the skin, as a result of tissue respiration, continuously produces free radicals. Both external and internal environmental factors can lead to disruption of the dynamic balance in the body's natural antioxidant defense system, reducing the potential of its biological capacity. The phospholipid layer of the cell membrane, nuclear and mitochondrial DNA can be exposed to aggressive action of free radicals, thereby causing or aggravating the existing pathology of the skin. Reduced biological activity of enzymatic and non-enzymatic components of the body's antioxidant defense system does not properly lead to the deactivation of free radicals, which requires other approaches to local therapy.

Oxidative stress (OS) is the imbalance between the generation of reactive oxygen species (ROS) and the body's antioxidant defenses in favor of ROS. ROS are chemical species that can be neutralized by natural phytochemicals like phenolic compounds present in medicinal plants and whose extraction depends on the solvent system used. Thus, the present study aimed to evaluate the effect of two extraction solvents on the polyphenols content and antioxidant activity of Alstonia boonei barks. For this, the bark of A. boonei were harvested, processed, dried and ground, then the powder was macerated in two solvent systems (water and water-ethanol). Subsequently, the quantitative phytochemical analysis of the different extractions was done by evaluating total polyphenols content (TPC), total flavonoids content (TFC) and alkaloids; followed by an in vitro evaluation of the antioxidants activity through radicals scavenging (DPPH and NO.) and the reducing power of ferric iron to ferrous iron. The relationship between antioxidant potential (DPPH, NO and FRAP) and polyphenols (total polyphenols and total flavonoids) was investigated using simple linear regression. It appears that the aqueous extract allowed better extraction of phenolic compounds from A. boonei bark; and exhibited better antioxidant activity. In addition, a strong correlation (r and R2) was found between polyphenols (TPC and TFC) and antioxidant activity (DPPH, NO and FRAPP). Thus, we preferably recommend the use of water as a solvent for traditional preparations of A. Boonei bark extract for therapeutic purposes.

Hypoxia is known to stimulate reactive oxygen species (ROS) generation. Because reduced glutathione (GSH) is compartmentalized in cytosol and mitochondria, we examined the specific role of mitochondrial GSH (mGSH) in the survival of hepatocytes during hypoxia (5% O2). 5% O2 stimulated ROS in HepG2 cells and cultured rat hepatocytes. Mitochondrial complex I and II inhibitors prevented this effect, whereas inhibition of nitric oxide synthesis with Nomega-nitro-L-arginine methyl ester hydrochloride or the peroxynitrite scavenger uric acid did not. Depletion of GSH stores in both cytosol and mitochondria enhanced the susceptibility of HepG2 cells or primary rat hepatocytes to 5% O2 exposure. However, this sensitization was abrogated by preventing mitochondrial ROS generation by complex I and II inhibition. Moreover, selective mGSH depletion by (R,S)-3-hydroxy-4-pentenoate that spared cytosol GSH levels sensitized rat hepatocytes to hypoxia because of enhanced ROS generation. GSH restoration by GSH ethyl ester or by blocking mitochondrial electron flow at complex I and II rescued (R,S)-3-hydroxy-4-pentenoate-treated hepatocytes to hypoxia-induced cell death. Thus, mGSH controls the survival of hepatocytes during hypoxia through the regulation of mitochondrial generation of oxidative stress.

Reactive oxygen species and nuclear factor-kappa B pathway mediate high glucose-induced Pax-2 gene expression in mouse embryonic mesenchymal epithelial cells and kidney explants

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder that significantly increases the risk of cardiovascular disease, which is the leading cause of morbidity and mortality among diabetic patients. A central pathophysiological mechanism linking T2DM to cardiovascular complications is oxidative stress, defined as an imbalance between reactive oxygen species (ROS) production and the body's antioxidant defenses. Hyperglycemia in T2DM promotes oxidative stress through various pathways, including the formation of advanced glycation end products, the activation of protein kinase C, mitochondrial dysfunction, and the polyol pathway. These processes enhance ROS generation, leading to endothelial dysfunction, vascular inflammation, and the exacerbation of cardiovascular damage. Additionally, oxidative stress disrupts nitric oxide signaling, impairing vasodilation and promoting vasoconstriction, which contributes to vascular complications. This review explores the molecular mechanisms by which oxidative stress contributes to the pathogenesis of cardiovascular disease in T2DM. It also examines the potential of lifestyle modifications, such as dietary changes and physical activity, in reducing oxidative stress and mitigating cardiovascular risks in this high-risk population. Understanding these mechanisms is critical for developing targeted therapeutic strategies to improve cardiovascular outcomes in diabetic patients.

Xanthohumol ameliorates lipopolysaccharide (LPS)-induced acute lung injury via induction of AMPK/GSK3β-Nrf2 signal axis

Mutant tp53 Causes a Gain of Function Increase in Sensitivity to Reactive Oxygen Species in Erythroid Precursors

As ultraviolet (UV) radiation is naturally and ubiquitously emitted by the sun, almost everyone is exposed to it on a daily basis, and it is necessary for normal physiological function. Human exposure to solar UV radiation thus has important health implications. The generation of reactive oxygen species (ROS) by UV radiation is one of the mechanisms through which UV light can manifest its possible detrimental effects on health. When an imbalance develops due to ROS generation exceeding the body's antioxidant defence mechanisms, oxidative stress can develop. Oxidative stress can lead to cellular damage (e.g. lipid peroxidation and DNA fragmentation), apoptosis and cell death. Broadly UV can induce ROS by affecting the cellular components directly or by means of photosensitization mechanisms. More specifically UV light can induce ROS by affecting the enzyme catalase and up-regulating nitric oxide synthase (NOS) synthesis. It may also cause a decrease in protein kinase C (PKC) expression leading to increased ROS production. UVR is capable of modifying DNA and other chromophores resulting in elevated ROS levels. The effects of raised ROS levels can vary based on the intracellular oxidant status of the cell. It is therefore important to protect yourself against the potentially harmful effects of UV light as it can lead to pathological UV-induced ROS production.

Oxidative stress is a critical pathological mechanism implicated in the progression of various disease conditions, primarily due to the excessive production of reactive oxygen species (ROS) that overwhelm the body's antioxidant defenses. Among the different cell types affected, erythrocytes are particularly vulnerable to oxidative damage because of their high polyunsaturated fatty acid content and continuous exposure to oxygen. This makes them a key target for oxidative injury, which can compromise membrane integrity and reduce cell lifespan. Natural antioxidants have gained considerable attention for their potential to mitigate oxidative stress. Fenugreek (Trigonella foenum-graecum), in particular, is recognized for its strong antioxidant properties, attributed to its rich composition of carotenoids, polyphenolic acids, and flavonoids. These bioactive compounds can effectively scavenge free radicals, thereby protecting erythrocytes from oxidative insult. The present study was to explore the antioxidant efficacy of Fenugreek in counteracting sodium fluoride-induced oxidative stress within sheep red blood cells (RBCs). The inherent vulnerability of RBCs to oxidative stress is attributed to the elevated presence of polyunsaturated fatty acids within their membranes. By subjecting red blood cells to 24-hour incubation with sodium fluoride (NaF), oxidative stress was effectively induced. Our protective strategies involved the utilization of ascorbic acid and Fenugreek extract. Notably, alterations in the levels of SOD, GSH, and MDA were utilized as indicators of oxidative stress severity. Both ascorbic acid and Fenugreek extract exhibited the capacity to restore the proportions of SOD, GSH, and MDA to levels parallel to the normal state. This resounding outcome underscored the potential of these treatments to mitigate the oxidative stress triggered by sodium fluoride (NaF) in erythrocytes. In conclusion, the pronounced antioxidant properties of both ascorbic acid and Fenugreek offer a promising avenue for alleviating the oxidative stress inflicted on erythrocytes by sodium fluoride (NaF). This study further accentuates the significant role of Fenugreek as a potential natural remedy against oxidative damage, particularly in the context of sodium fluoride-induced stress within red blood cells.

Oxidative stress mediates ethanol-induced skeletal muscle mitochondrial dysfunction and dysregulated protein synthesis and autophagy

This study evaluates the health of a captive colony of Hamadryas baboons at Ravenna Zoo Safari (Italy), focusing on oxidative stress markers and biometric data. Forty-eight individuals were assessed during routine veterinary procedures: males underwent vasectomy, and females were checked for pregnancy. Biometric data collected included body weight, body length, and genital measurements in males, while females were evaluated for reproductive status. Oxidative stress was measured using two tests that assess both harmful pro-oxidant levels and the body's antioxidant defenses. Results showed no significant differences in oxidative stress levels between sexes, although males and females differed in body weight. Pregnant and postpartum females exhibited higher oxidative stress, likely due to the metabolic and hormonal demands of reproduction. This supports the idea that reproductive activity increases the production of reactive oxygen species, requiring stronger antioxidant responses. In males, correlations between body weight and genital measurements suggest these could help estimate age in the absence of birth records. No link was found between oxidative stress and body weight, indicating limited age-related effects on these markers. Overall, the study highlights the importance of monitoring oxidative stress in captive primates to better understand the effects of reproduction and aging, and to improve welfare and management practices.

Background: Chronic diseases are increasingly prevalent worldwide, with lifestyle choices playing a significant role in their management. Free radicals and oxidative stress have been implicated in various chronic conditions, including cardiovascular diseases, cancer, and neurodegenerative disorders. These conditions arise from an imbalance between reactive oxygen species (ROS) production and the body's antioxidant defenses. Aim: This review aims to explore how lifestyle choices influence oxidative stress and chronic disease management, with a focus on the role of healthcare providers in guiding lifestyle modifications to mitigate oxidative stress and improve health outcomes. Methods: A comprehensive review of the literature was conducted, focusing on the mechanisms of oxidative stress and its impact on chronic diseases. Studies on the effects of lifestyle factors such as diet, exercise, smoking, and alcohol consumption on oxidative stress were analyzed. The role of antioxidants in counteracting oxidative damage and their implications for chronic disease management were also examined. Results: The review highlights that lifestyle factors significantly affect oxidative stress levels. Moderate exercise enhances antioxidant defenses, while excessive physical activity, smoking, and alcohol consumption exacerbate oxidative stress. A diet rich in antioxidants helps mitigate oxidative damage.

Abstract: In the past decade, oxidative stress, characterized by an imbalance between reactive oxygen species (ROS) production and the body's antioxidant defenses, has emerged as a pivotal factor in the pathogenesis of various pregnancy complications. This condition poses significant clinical challenges, impacting maternal and fetal health. This review aims to comprehensively explore the clinical and biological implications of oxidative stress during pregnancy. It investigates how oxidative stress influences pregnancy outcomes, emphasizing its relevance in prenatal care and management. A rigorous literature review encompassed peer-reviewed journals, clinical studies, and meta-analyses examining oxidative stress in pregnancy. The analysis reveals a consistent association between oxidative stress and complications such as preeclampsia, gestational diabetes, and intrauterine growth restriction. Elevated ROS levels and reduced antioxidant capacity were consistently observed in affected pregnancies, contributing to endothelial dysfunction, inflammation, and impaired placental function, thereby adversely affecting maternal and fetal health. Understanding the role of oxidative stress in pregnancy-related complications is crucial for developing effective preventive and therapeutic strategies. Highlighting the significance of antioxidant defenses in prenatal care can potentially enhance management practices and improve health outcomes for both mothers and infant. Keywords: Oxidative stress, Reactive oxygen species (ROS), Antioxidant, Pregnancy complications and maternal health.