The development of reproducible rodent models of coronary microvascular disease (MVD) is essential for the early detection, treatment, and mechanism study of the pathophysiology. We hypothesized that endothelial dysfunction and subsequent microthrombi in the coronary arterioles, two early events in clinical coronary MVD, could be reproduced by photochemical reaction (PCR) technology in mice hearts. After rose bengal (one of photosensitizers) was administrated systemically, a green light was locally used to activate the photosensitizer, inducing over-production of oxidative stress in the heart. Following PCR, animals demonstrated reproducible endothelial injury, occlusion in arterioles, focal ischemia, and infarct-let with preserved cardiac function. Our technique has proven to be a reliable and reproducible means of creating coronary MVD in mice. We believe that this is an ideal model for developing a novel molecular tracer for earlier detection of coronary MVD, for testing new anti-fibrinolytic drugs, and for investigating the complex pathophysiology of coronary MVD. The protocol for establishing this model takes about thirty to forty minutes.

Background: Dysmenorrhea is menstrual disorder that affects about 40% - 90% of women worldwide, it is associated with oxidative stress. The current treatment of this condition is administration of non-steroidal anti-inflammatory drugs, which when frequently used, may affect organs. Objective: Assess the hepatotoxicity and nephrotoxicity side effects related to dysmenorrhea and its treatment Materials and methods: A survey (questionnaire) was designed and implemented on 689 female students of the University of Dschang. After this, and following the inclusion criteria, 191 blood samples were collected for assay of hepatotoxicity markers (transaminases, albumin), nephrotoxicity indicators (creatinine, urea, total protein) and the inflammation associated indicators. The measurements were performed on fully automated Olympus AU 400 Analyzer, using standard reagent kits. Results: Subjects with untreated dymenorrhea lasting more than five years had a significantly high level (p < 0.05) of ALT (39.47 ± 15.74 IU/L) and AST (44.37 ± 13.74 IU/L). Transaminases levels were significantly associate (p < 0.01) and positively correlate (0.251 for ALT and 0. 223 for AST) with the disease duration. Dysmenorrheic individuals on medication for more than 9 years had significantly higher ALT (25.14 ± 7.85 IU/L) and AST (35.26 ± 0.70 IU/L) levels (p < 0.05) compared to those under treatment for less than 5 years (19.37 ± 8.27 UI/L and 27.68 ± 8.56 UI/L). The use of analgesics, regardless of the duration of treatment, had normal creatinine clearance (107.44 ± 30.86 ml/min), compared to those treated with either anti-inflammatory drugs (71.56 ± 26.44 ml/min), or a combination of analgesics and anti-inflammatory drugs (81.34 ± 31.97 ml/min), which was significantly reduced (p < 0.05). Conclusion: Dysmenorrhea duration, type and duration of treatment potentially expose participants to liver and kidney disorders.

In various patients conditions involved in lower urinary tract disease LUT (like overactive bladder, bladder neck sclerosis, dis –synergy (with our synenrgic contraction between bladder detrusor and bladder neck, BPH, recurrent cysytitis, interstitial cystitis, chronic prostatitis, uretral stenosys, loss of sfinteric coordination. Prostatic cancer, anatomic abnormalities and other the receptor status play relevant role to reduce effect of vicious clycle that can be responsible in progression of the pathologic process. In this work the complex receptorial status is analyzed to verify new therapeutic strategies. Starting from the observation that various irritant substanties produce irritant stimulus in Prostatic Patients or in bladder neck condition is interesting to deep understand the etio-patogenesys and Functional results. In Various prostatic, bladder neck or ureteral condition a reduced urinary fluss can produce infectious. Conditions like acute or chronic prostatitis. Irritants sustanties in diet (in example etilic alcohol drink, hot spices, crud meats, carbonate drinks, caffeine and other) can produce Painful stimulus in innervations of vecical trigonous, bladder neck and prostatic urethra. The same recurrent cystitis and Bph contribute in a complex situation. This stimulus produce ipertonus of bladder muscle involved in the expulsion of urine. The event related inflamation and edema (bladder, prostatic uretra, trigonus) contribute to the global effect. So conditions like bladder neck sclerosys IPB, recurrent prostatitis and cistitys in acts in a vicious circle. (Also immunomediated: Bph and cronic prostatitis with linfocite infiltration and tissue remodeling). The ormonal status check the systems (see 5-ARI efficacy in Bph). Simpatic, parasimpatic and other system are deeply involved. Also behavioral habits or diet can influence in example urinary flux in a complex system like LUT. (Bladder and prostatic irritants that can produce edema and acute inflamation). Other behavior habits are deeply involved as too much sedentary, water intake, coffee, pee modality and also psychological profile and stressing conditions. Some disease like diabetes produce high consequences in all this systems due to Bladder modification, oxidative stress, osmotic movens, and increase susceptibility of urinary infections. This article are verified this kind of movens that contribute in physio -pathology of some low urinary tract conditions. The anatomic abnormalities produces, obviously, physiological disfuntions. Recurrent urinary tract infections, inadequate antimicrobial therapy: Profile of resistance, duration of therapy, kind of antimicrobials, posology, Pk. Kinetics, associations, compliance, biofilms, micro calcifications (recurrent chronic prostatitis) contribute to a progression of the condition.

Emerging evidence indicates that micronutrient deficiency could play a significant role in the pathogenesis and progression of many chronic diseases including diabetes mellitus, hypertension, obesity, dyslipidemia, hyperuricemia, kidney disease, cancer, anemia and other cardio-metabolic and neurodegenerative diseases through the induction of Insulin resistance (IR). However, there are still gaps in our scientific knowledge regarding the links between micronutrient deficiencies, IR, and cardio metabolic disorders. This review provides current information on recent advances and a global perspective regarding the relationship between micronutrient deficiency, IR, and cardio metabolic disorders. Empirical evidence indicates that deficiencies in either micronutrients associated with insulin activity (such as Chromium, manganese, magnesium, and iron) or antioxidant enzyme cofactors (such as vitamin A, copper, zinc, and manganese) could impact several physiological processes leading to a cascade of metabolic and biochemical derangements such as B-cell apoptosis, loss of islet cell mass, defective tyrosine kinase activity, oxidative stress, pancreatic β-cell dysfunction, reduction in lean body mass, defective insulin signaling mechanism, elevated protein kinase C activity, and excess intracellular calcium. Collaboratively, these states of metabolic malfunctioning are associated with IR, which triggers the onset of many cardio metabolic diseases. Undoubtedly, the prevention of micronutrient deficiency may indeed ameliorate the incidence of IR and cardio-metabolic disorders in those at risk and in the general population.

In COVID-19 pandemic we focused on epidemiology and somewhat we neglect the possibility of biochemical influencing of the infection. Therefore we try to find some properties of the virus, which are impressionable by drugs. Droplet infection transmission is mainly (hypochloric acid) by nose and mouth. Diseases of nose and paranasal sinuses are most often of viral or bacterial origin.

Background: Cyclophosphamide is used for the treatment of malignant and non-malignant diseases, but, it induces oxidative damage and disturbance in the antioxidant defense system. Zinc oxide nanoparticles (ZnO NPs) are used in biomedical applications and consumer products. ZnO-NPs are protected cell membranes against oxidative damage, decrease free radicals and malondialdehyde (MDA) levels, and increase the antioxidant enzyme levels. Objectives: The present aimed to evaluate the ameliorative effect of Zn-O nano-particles on oxidative damage and disturbance in the antioxidant defense system induced by cyclophosphamide in male albino rats. Materials and Methods: 24 adult male albino rats were randomly divided into 4 groups (6 rats of each). Group I (Control group): Received 0.2 ml saline /day i.p. injection for 14 days (day by day), group II, (nZnO group): Received nZnO (5 mg/kg/day) b.w., intraperitoneally for 14 days, Group III (CP group): Received CP (20 mg/kg/day) b.w, day by day for 14 days by intraperitoneal injection, Group IV (CP + ZnO NPs group): Received nZnO group: Received nZnO (5 mg/kg/day) b.w., intraperitoneally for 14 days, plus CP (20 mg/kg/day) b.w., day by day for 14 days by intraperitoneal injection. After 24-hr from the last treatment, all animals were anesthetized using light ether. Blood, lungs, and liver samples were taken and prepared for biochemical measurements. Results: Individual treatment of zinc oxide nanoparticles and CP induced liver cytochrome b5, cytochrome C reductase, and glutathione S-transferase (GST) compared to the control group, while CP increased P450. The combination of nZnO and CP prevents the elevation of cytochrome b5, P450, cytochrome C reductase, and GST compared with the CP treated group. Zinc oxide nanoparticles and CP increased liver thiobarbituric acid reactive substances (TBARS). The combination of nZnO and CP prevents the changes in TBARS concentrations compared with the CP. Injection of CP to rats reduced the activities of serum glutathione reductase (GR) and catalase (CAT) as compared with the control group. However, combination treatment of rats with nZnO and CP increased the activities of these enzymes compared with those treated with CP alone. Zinc oxide nanoparticles and CP increased serum and lung TBARS, while decreased glutathione (GSH) concentration compared to the control group, with more pronounced changes by CP. The combination of nZnO and CP prevents the changes in TBARS and GSH concentrations compared with the CP. Conclusion: It can be concluded that CP induced oxidative stress and disturbance in the antioxidant defense system. Treatment of rats with zinc oxide nano-particles and CP together attenuated the oxidative damage and disturbance in the antioxidant defense system induced by CP. So, Patients treated with CP advised to take nZnO to prevent the side effects of chemotherapy. Further studies are necessary to evaluate the amelioration effect nZnO and other nano-particles against oxidative stress induced by CP in different doses and experimental models.

Nearly all energy production in living organisms is by oxidation reactions (fires are large oxidative embers) Oxidation reactions produce, through complex intermediate steps, small energy packages that are more easily stored than a sudden combustion oxidation. The slow and controlled production of energy in a nuclear power plant allows its use, a massive explosion produces the result that we know ... It’s the same thing in our bodies. These reactions are never 100% efficient, not all the energy produced is used as bio fuel. Indeed, during the intermediate stages, they induce a deterioration of cells and tissues by consuming about 10% of this energy. They cause significant “wear and tear” when there is no longer any compensation for these parasitic oxidations. The latter can be excessively used in pathological situations inducing inflammatory reactions, or simply during metabolic overproduction, or even simple intense and prolonged efforts.

High blood pressure (HBP) is a strong, independent and etiologically relevant risk factor for cardiovascular and therefore, the leading cause of preventable deaths worldwide. Hypertension has high medical and social costs. Due to its many associated complications, the use of medical services create high costs with medications which represent almost half of the estimated direct expenses. Free distribution of more than 15 medications for HyPERtension and DIAbetes (HIPERDIA program) clearly shows the important role of drugs in the Brazilian Government’s effort to tackle these two diseases. Notwithstanding, the prevalence of HBP is rising in parallel with other NCDs. It is known that HBP results from environmental and genetic factors, and interactions among them. Our ancestors were often faced with survival stresses, including famine, water and sodium deprivation. As results of natural selection, the survival pressures drove our evolution to shape a thrifty genotype, which favored/promoted energy-saving and sodium/water preservation. However, with the switch to a sodium- and energy-rich diets and sedentary lifestyle, the thrifty genotype and ancient frugal alleles, are no longer advantageous, and may be maladaptive to disease phenotype, resulting in hypertension, obesity and insulin resistance syndrome. Low-grade chronic inflammation and oxidative stress would be the underlying mechanisms for these diseases. HBP is often associated with unhealthy lifestyles such as consumption of high fat and/or high-salt diets and physical inactivity. Therefore, alternatively to medicine drugs, lifestyle and behavioral modifications are stressed for the prevention, treatment, and control of hypertension. A lifestyle modification program (LSM) involving dietary counseling and regularly supervised physical activity (“Move for Health”) has been used for decades, in our group, for NCDs primary care. Retrospective (2006-2016) data from 1317 subjects have shown the top quartile of blood pressure(142.2/88.5mmHg) differing from the lower quartile (120.6/69.2mmHg) by being older, with lower schooling, lower income and, lower physical activity and aerobic capacity. Additionally, the P75 showed higher intake of CHO, saturated fat and sodium along with lower-diet quality score with a more processed foods. They showed higher body fatness and prevalence of metabolic syndrome along with higher pro-inflammatory and peroxidative activities and insulin resistance. In this free-demand sample, the HBP rate was 51.2% for SBP and 42.7% for DBP. The rate of undiagnosed HBP was 9.8% and only 1/3 of medicated patients were controlled for HBP. After 10 weeks of LSM the HBP normalization achieved 17.8% for SBP and 9.3% for DBP with a net effectiveness of 8.5% and 2.4%, respectively. The reduction of HBP by LSM was followed by increased aerobic conditioning and reduced intake of processed foods along with decreased values of BMI, abdominal fatness, insulin resistance, pro-inflammatory and peroxydative activities. Importantly, once applied nationwide this LSM would save HBP medication for 3.1 million of hypertensives at an economic saving costs of US$ 1.47 billion a year!

In this review After Observing biomedical literature (starting from some heart disease) results that some pathological phenomena are deeply involved in some metabolic endocrine condition: Kinetics and gradients in metabolism, catabolism, time related, toxic like effect, electrical cell membrane status, smooth vascular muscle cell hyper-reactivity, platelet iperactivations, central autonomic control after acute stroke, great electrolytes unbalances et other factors as pro-hypertrophic signaling and oxidative stress. Observing actual current therapy in some metabolic endocrine therapy often is used association of drugs (in example in type II diabetes). In Many other pathologies efficacy drug therapy exist, and often only 1 pharmacological molecule resolve the pathological condition. But in many disease even associating 2-3-4 drugs the % of cure not increase (efficacy, effectiveness). It mean that this drugs strategies are not the really best? Or it mean a low active level? Why for this pathological condition this association drugs in currently use not do the right works as really needed? There is the need for new really efficacy drugs strategy that show a profile of efficacy as requested in order to resolve the pathological condition? Or to be added to the actual therapy? The actual pharmacological strategies in some metabolic endocrine disorder is really the best? Or other strategies can be introduced?

Zinc induced pediatric preventing respiratory 2019-nCoV is required that supplementation with zinc gluconate 20 mg in Zn deficient children resulted in a nearly twofold reduction of acute lower respiratory infections as well as the time to recovery. Zinc supplementation in children is associated with a reduction in the incidence and prevalence of pneumonia. Preventing 2019-nCoV pneumonia is required that zinc supplementation alone (10 to 20 mg) for more than 3 months significantly reduces in the rate of pneumonia. zinc pediatric intake may be required to be effective range 10～20 mg/d for 2019-CoV prevention, 10～30 mg/d for reduction of COVID-19 bronchitis, and 20～30 mg/d for recovery from COVID-19 pneumonia, in which Zn2+ could bind with viral surface proteins by Zn2+ions-centered tetrahedrally coordination pattern. On the other hand, for aults, the zinc-homeostatic immune concentration may provide a protective role against the COVID-19 pandemic, likely by improving the host’s resistance against viral infection. 50 mg of zinc per day might provide an additional shield against the COVID-19 pandemic, possibly by increasing the host resistance to viral infection to minimize the burden of the disease. In order to prevent that an outbreak of respiratory sickness caused by a novel coronavirus (COVID-19) has become a serious public threat and disrupted many lives,assessing the efficacy of FDA-approved Zn-ejector drugs such as disulfiram combined with interferon to treat COVID-19 infected patients has been proposed. The key strategies for preventing lung damages include avoiding direct lung infection, altering host-virus interactions, promoting immune responses, diluting virus concentrations in lung tissues by promoting viral migration to the rest of the body, maintaining waste removal balance, protecting heart function and renal function, avoiding other infections, reducing allergic reactions and anti-inflammatory. The interactions had been found on the binding specificity by Zn2+ ions-centered tetrahedral geometric coordination of the inhibitors against 3C and 3C-like proteases. In addition, transient zinc chelation TPEN and EPDTC have been noted as preventing virus replication. Zinc-induced ROS production in COVID-19 respiratory ailment and pneumonia occurs both in children and adults. In children. ROS production in zinc (Ⅱ)-immune pediatric patient with COVID-19 bronchitis and pneumonia cannot be elucidated yet. In adults, zinc induced ROS generation in pulmonary COVID-19 infected cells is that alterations of ROS-producing and scavenging pathways that are caused by respiratory viral infections are implicated in inflammation, lung epithelial disruption, and tissue damage, and, in some cases, even pulmonary fibrosis. The involvement of oxidative stress in cell deaths caused during RNA virus infection and ROS production is correlated with host cell death.

Increased exposure to electromagnetic fields such as radio frequencies used by Wifi technology raise questions and concerns about their impact on health. For answer these questions, several scientific studies have carried out followed by results publication in prestigious scientific revues. Literature conducted on the effects of non-ionizing radiation and Wifi waves is vast and sometimes controversial. Epidemiological studies and the results of in vitro and in vivo experimental studies have showed the biological effects of electromagnetic field in different frequencies range. These effects caused disorders at the molecular and behavioral level. However, these studies were insufficient to confirm the directly related effects to the cause. Therefore, further research must be done to raise the controversy about the safety of wireless waves.

The biological changes caused by oxidative stress (OS) are known to be involved in the etiology of neurodegenerative disorders, including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Parkinson’s disease. The brain is particularly vulnerable to OS due to its high lipid content and extensive consumption of oxygen. OS processes, particularly the excessive production of reactive oxygen species (ROS), play a critical role in how neurodegenerative disorders develop. This is evidenced by in vivo studies investigating various biomolecules related to OS, such as products of lipid and DNA oxidation. Accordingly, ROS can also cause oxidative-related damage in neurodegenerative disorders, including dopamine auto-oxidation, mitochondrial dysfunction, glial cell activation, α-synuclein aggregation, excessive free iron, and changes in calcium signaling. Furthermore, excessive levels of cellular oxidants reduce antioxidant defenses, which in turn propagate the cycle of OS. As such, it is increasingly important to determine the linkage between a high intake of antioxidants through dietary interventions and a lower risk of developing neurodegenerative diseases. Indeed, in addition to modulating the immune system, optimal nutritional status is capable of changing various processes of neuroinflammation known to be involved in the pathogenesis of neurodegeneration. Accordingly, a better understanding of the role ROS plays in the etiology of neurodegeneration is needed, along with the identification of dietary interventions that may lead to improved therapeutic strategies for both the treatment and prevention of neurodegenerative disorders. Therefore, this review presents a comprehensive summary of the role of ROS in the pathogenesis of neurodegenerative disorders. In addition, nutrients believed to be useful for mitigating and counteracting ROS are discussed. 

Protein phosphorylation regulates several dimensions of cell fate and is substantially dysregulated in pathophysiological instances as evident spatiotemporally via intracellular localizations or compartmentalizations with discrete control by specific kinases and phosphatases. Cardiovascular disease manifests as an intricately complex entity presenting as a derangement of the cardiovascular system. Cardiac or heart failure connotes the pathophysiological state in which deficient cardiac output compromises the body burden and requirements. Protein kinases regulate several pathophysiological processes and are emerging targets for drug lead or discovery. The protein kinases are family members of the serine/threonine phosphatases. Protein kinases covalently modify proteins by attaching phosphate groups from ATP to residues of serine, threonine and/or tyrosine. Protein kinases and phosphatases are pivotal in the regulatory mechanisms in the reversible phosphorylation of diverse effectors whereby discrete signaling molecules regulate cardiac excitation and contraction. Protein phosphorylation is critical for the sustenance of cardiac functionalities. The two major contributory ingredients to progressive myocardium derangement are dysregulation of Ca2+ processes and contemporaneous elevated concentrations of reactive oxygen species, ROS. Certain cardiac abnormalities include cardiac myopathy or hypertrophy due to response in untoward haemodynamic demand with concomitant progressive heart failure. The homeostasis or equilibrium between protein kinases and phosphatases influence cardiac morphology and excitability during pathological and physiological processes of the cardiovascular system. Inasmuch as protein kinases regulate numerous dimensions of normal cellular functions, the pathophysiological dysfunctionality of protein kinase signaling pathways undergirds the molecular aspects of several cardiovascular diseases or disorders as related in this study. These have presented protein kinases as essential and potential targets for drug discovery and heart disease therapy.

Psoriasis is a chronic inflammatory skin disease with a complex mechanism, which is believed to be mainly based on immune disorders and activation of inflammatory pathways. However, we have combed through the literature and found that the pathogenesis of psoriasis might involve a “mobius loop” of “immunity-inflammation-oxidative stress-proliferation” process. The disordered immune environment of the skin might act as the basis, the outbreak of inflammatory factors as the mediator, and the imbalance of oxidative stress homeostasis as the activator. These factors work together, leading to abnormal proliferation of keratinocytes and further immune abnormalities, finally aggravating psoriasis. Therefore, here we review the latest evidence and advance in the pathogenesis of psoriasis, trying to contribute to further understanding and treatment of psoriasis.

Air pollution exposure is among the most prevalent reasons for environmentally-induced oxidative stress and inflammation, both of which are implicated in the central nervous system (CNS) diseases. The CNS has emerged as an important target for adverse health effects of exposure to air pollutants, where it can cause neurological and neurodevelopmental disorders. Air pollution includes various components of gases, particulate matter (PM), ultrafine particulate (UFPs), metals, and organic compounds. An important source of PM and UFPM in the ambient air is associated with air pollution-related trafficking, and primarily diesel exhaust particles (DEPs). Controlled animal studies and epidemiological studies show that exposure to air pollution, and in particular urban air pollution or DEPs, may lead to neurotoxicity. In specific, exposure to air pollutants as an important factor may be in neurodevelopmental disorders (eg Autism) and neurological disorders (eg.., Alzheimer’s Disease (AD)). The most noticeable effects of exposure to air pollutants in animals and humans are oxidative stress and neurodegeneration. Studies in rats exposed to DEPs showed microglial activity, increased lipid peroxidation, and neuronal accumulation in various areas of the brain, especially the olfactory bulb (OB) and the hippocampus (HI). Disorders of adult neurogenesis were also found. In most cases, the effects of DEP are more pronounced in male mice, probably due to lower antioxidant capacity due to less expression of paraoxonase 2.

Introduction: Oxidative stress is a phenomenon induced by an imbalance between production and the biological system's ability to readily detoxify oxygen reactive species (ROS) in cells. It has been shown that grape juice can reduce oxidative stress due to the presence of polyphenols. The aim of this study was to evaluate the effect of fresh red grape juice and grape fermentative product on oxidative stress in human erythrocytes.Methods: 5 ml of blood from 125 healthy individuals as control group collected in EDTA containing tubes. To perform biochemical assays, erythrocytes were incubated at 37 ºC for different times including 4, 24, 48, and 72 hours in the presence or absence of grape juice and grape red wine in amounts of 5 ml. Results: Grape juice and grape red wine reduced lipid peroxidation and increase of thiol groups, and total antioxidant capacity after 24 hours of treatment (p < 0.05). Also, the activity of catalase enzyme was increased 4 and 24 hours after treatment with red wine and grape juice, respectively. Conclusion: Grape juice and grape fermentative product may improve the antioxidant power of erythrocytes. This may lead to reducing the risk of free-radical damage and chronic diseases. However, more research with a higher number of samples is necessary to confirm the antioxidant effect of grape juice and red wine on human erythrocytes.

The commonest etiology of acute kidney injury (AKI) is Sepsis that results in an escalation of morbidity and mortality in the hospital intensive care units. Existentially, the therapy of septic AKI rather than being definitive or curative is just supportive, without tackling the pathophysiology. Usually, Sepsis gets correlated with systemic inflammation, along with the escalated generation of Reactive oxygen species (ROS), in particular superoxide. Simultaneously liberation of nitric oxide (NO) subsequently reacts with the superoxide, thus, resulting in the generation of reactive nitrogen species (RNS), that is mostly peroxynitrite. This sepsis stimulated generation of ROS in addition to RNS might cause a reduction in the bioavailability of NO that modulates microcirculation aberrations, localized tissue hypoxia as well as mitochondrial impairment, thus starting a vicious cycle of cellular damage which results in AKI. Here we conducted a systematic review utilizing search engine PubMed, Google scholar; Web of science; Embase; Cochrane review library utilizing the MeSH terms like septic AKI; ROS; inducible nitric oxide synthase (iNOS); nicotinamide adenine nucleotide phosphate(NADPH)oxidase complex; Oxidative stress; Renal medullary hypoxia; Hypoxia inducible factor1; hypoxia responsive enhancer A; mitochondrial impairment; Intrarenal oxygenation; urinary oxygenation; erythropoietin gene; RRT; NAC; Vitamin C from 1950 to 2021 till date. We found a total of 6500 articles out of which we selected 110 articles for this review. No meta-analysis was done. Thus here we detail the different sources of ROS, at the tie of sepsis, besides their pathophysiological crosstalk with the immune system, microcirculation as well as mitochondria that can result in the generation of AKI. Furthermore, we detail the therapeutic utility of N-acetylcysteine (NAC), besides the reasons for its success in ovine as well as porcine models of AKI. Moreover, we discuss preclinical along with clinical for evaluation of Vitamin C’s antioxidant effects as well as pleiotropic effects as a stress hormone that might aid in abrogation of septic AKI.

Neurological disorders are a significant cause of mortality and disability across the world. The current aging population and population expansion have seen an increase in the prevalence of neurological and psychiatric disorders such as anxiety, bipolar disorder, depression, epilepsy, multiple sclerosis and schizophrenia. These pose a significant societal burden, especially in low - and middle-income countries. Many neurological disorders have complex mechanisms and lack definitive cures; thus, improving our understanding of them is essential. The pathophysiology of neurological disorders often includes inflammation, mitochondrial dysfunction and oxidative stress. Oxidative stress processes, especially the generation of reactive oxygen species, are key mechanisms in the development of neurological disorders. Oxidative stress refers to an imbalance between the production of reactive oxygen species and antioxidants that can counteract them. Through their impacts on the pathophysiology of neurological disorders, nutrients with anti-inflammatory, neuroprotective and antioxidative properties have been suggested to prevent or mitigate these disorders. Certain vitamins, minerals, polyphenols and flavonoids may have therapeutic effects as adjuvant treatments for neurological disorders. Diet quality is also a risk factor for some neurological and psychiatric disorders and addressing nutritional deficiencies may alleviate symptoms. Therefore, optimizing nutritional intake may represent a potential treatment or prevention strategy. This review summarizes a selection of promising nutrients for the prevention and amelioration of neurological disorders to provide a summary for scientists, clinicians and patients, which may improve understanding of the potential benefits of nutrients in the treatment of neurological disorders.

Parkinson’s disease is a progressive and debilitating neurodegenerative disorder affecting millions of people worldwide. The disease is characterized by motor symptoms such as tremors, rigidity and postural instability, as well as non-motor symptoms such as depression and cognitive impairment. While there is no cure for Parkinson’s disease, there are various treatments available to manage symptoms and improve quality of life for patients.This case study examines a 65-year-old retired accountant, Mr. John Smith, who was diagnosed with Parkinson’s disease five years ago. Mr. Smith has been treated with a combination of medications, including levodopa and carbidopa and physical therapy to manage his symptoms. However, his symptoms have not significantly improved.This literature review explores the current research on Parkinson’s disease, including its pathophysiology, diagnosis and treatment. Parkinson’s disease is caused by the degeneration of dopamine-producing neurons in the brain, leading to a depletion of dopamine and the accumulation of alpha-synuclein protein, oxidative stress and inflammation. Diagnosis is based on clinical symptoms, neurological examination and response to dopaminergic therapy. Treatment focuses on managing symptoms, with medications and non-pharmacological interventions such as exercise and physical therapy. Deep brain stimulation is a surgical treatment option that has been shown to be effective in managing motor symptoms.While there is currently no cure for Parkinson’s disease, ongoing research into its pathophysiology and treatment holds promise for improving outcomes for patients. This case study highlights the importance of early diagnosis and personalized treatment plans for patients with Parkinson’s disease.

Oxidative stress has been implicated in Alzheimer’s and many other diseases and more recently, it has been linked to various COVID-19-related symptoms. Many diseases do not develop immediately as a result of the accumulated causes or injury, but rather, as a result of prolonged exposure to elevated oxidative stress, which disrupts the body’s natural homeostatic functions.