oxidative stress

Amyotrophic lateral sclerosis (ALS) disease is characterized by degeneration of motor neurons and elevation of brain oxidative stress. Previous studies demonstrated the neuroprotective effects of Telomerase reverse transcriptase (TERT) from oxidative stress. We showed that increasing TERT expression in the brain of the Tg hSOD1G93A mouse ALS model attenuated the disease pathology and increased the survival of motor neurons exposed to oxidative stress. How TERT increased the survival of motor neurons exposed to oxidative stress is not yet clear. Here we investigated the consequence of TERT depletion in motor neuron cells under normal and oxidative stress conditions and in mouse brains of TERT knockout mice, on the expression and activity of SOD1 and catalase enzymes. Depletion of mouse TERT caused mitochondrial dysfunction and impaired catalase and SOD1 activity. Compensation with hTERT restored the activity of SOD1. SOD1 expression increased in the brain of TERT KO and in ALS mice and decreased in the brain of WT mice treated with telomerase-increasing compounds. We suggest that the ability of TERT to protect neurons from oxidative stress affects the expression and activity of SOD1, in a TERT-dependent manner, and supports the notion of TERT as a therapeutic target for neurodegenerative diseases like ALS.

Introduction: The aim of this study was to examine the effects of Zn supplementation on oxidative stress by evaluating changes in serum Copper (Cu) to Zinc (Zn) ratio, homocysteine (hCys), Glutathione (GSH), Total Bilirubin (TB) and Catalase (CAT) activity in hemodialysis patients.Methods: Seventy-seven HD patients were enrolled in a multicenter simple-blind randomized clinical trial. Only 37 HD patients completed the study. They were randomly divided into two groups and supplemented with zinc sulfate (n = 17) or placebo (n = 20) for two months. Serum Zn and Cu were measured by atomic absorption spectrophotometry. Serum hCys was measured by immunology method, serum GSH and CAT activity were assessed by spectrophotometry method and TB was measured by colorimetric method. Determinations were performed before and after supplementation.Findings: After zinc supplementation, serum Zn, serum GSH, and Serum Total Bilirubin (STB) significantly increased. Serum Cu to Zn ratio, serum hCys, and CAT activity significantly decreased in the Zn Zn-supplemented group.Conclusion: Zinc supplementation increased serum antioxidant factors such as Zn, GSH, and bilirubin and decreased serum oxidative factors such as copper to zinc ratio, hCys, and decreased CAT activity. The study results suggest that zinc supplementation may be a useful tool for the improvement of oxidative stress in HD patients.

Background information: Cultural practices play an important role on the development of pathogens (Datnoff, et al. 2007). In this context, several authors have been interested in studying the effects of mineral nutrition on the resistance of vegetables and fruits to fungi during storage, especially nitrogen.The purpose of the study: In this work we tested the effects of three contrasted regimes of nitrogen supply, with nitrate concentrations in the nutrient solutions of 2 mM (low), 10 mM (normal) and 20 mM (high) on the susceptibility of Lactuca sativa L towards Botrytis cinerea (BC87) and Sclerotinia minor (SM) during storage.Once harvested, the outerleaves of the plants derived from the three nitrogen regimes were inoculated with either Botrytis cinerea (BC87) or Sclerotinia minor (SM). Data showed that the resistance to this two pathogens increase when plants were developed under low nitrogen concentration. This resistance observed is correlated with low values in oxidative stress indicators (MDA and H2O2) and high values in total phenols.

Introduction: In Sudan, Grewia tenax fruits, are known commonly as Goddaim. The fruit’s pericarp is used traditionally for a long time as a juice or a porridge to treat iron deficiency anemia (IDA). Traditional Goddaim users have a very strong belief in its effectiveness. However, the pattern of hemoglobin improvement follows an initial fast increase followed by a decline upon continuing its use. Some previous studies have attributed its effect to high iron content, while the iron quantity was too small. This work attempts to find an explanation for its mechanism of action by screening the fruit extract and its respective fractions for secondary metabolites, minerals, vitamins, and fibre. Methods: Entailed three methodologies: Chemical analysis to identify quantified minerals, ascorbic acid and non-digestible fibers, Phytochemical Analysis to separate and identify secondary metabolites using high-performance liquid chromatography coupled to tandem mass spectrometry (HPLC-MS-MS technique), and estimation of radical scavenging activities of crude fruit extract and its respective chloroform and ethyl acetate fractions by inhibition of the 2,2-diphenylpicrylhydrazyl (DPPH).Results: Ascorbic acid and indigestible fibres were revealed in the aqueous extract. Secondary metabolites were flavonoids (e.g., quercetin, kaempferol), organic acids (e.g., ferulic acid, chlorogenic acid), β-carboline alkaloids (e.g., 3-hydroxy-tetrahydroharman) identified in the chloroform, and ethyl acetate fractions. The in vitro antioxidant activity of G. tenax fruit extract was confirmed spectrophotometrically. Conclusion: It can be concluded that the initial enhancement of iron absorption through ascorbic acid and fibres, followed by iron uptake inhibition, could be explained by iron chelation by the chelators in the fruits. This paradoxical effect may qualify G. tenax fruits as a safety gauge for improving haemoglobin levels without compromising iron excess once iron stores are filled by keeping the oxidative stress in check. This may present G. tenax fruits as a good and safe remedy that optimizes the treatment of IDA.

Pregnancy complications present significant challenges, impacting maternal health and fetal development. Oxidative stress, a key contributor to various pregnancy-related disorders such as preeclampsia, gestational diabetes mellitus (GDM), and preterm birth, has spurred interest in exploring antioxidant interventions. Antioxidants, known for their ability to counteract oxidative damage, have emerged as potential therapeutic agents to mitigate these complications. This paper synthesizes current knowledge on the role of antioxidants in pregnancy, elucidating their mechanisms of action, sources, and impact on oxidative stress-related complications. It examines diverse antioxidant compounds, including vitamins C and E, selenium, and natural phytochemicals, highlighting their potential to modulate oxidative stress pathways and promote maternal-fetal well-being. Furthermore, this paper critically analyzes clinical studies, meta-analyses, and preclinical research exploring the efficacy and safety of antioxidant supplementation during pregnancy. It discusses the complexities surrounding optimal dosages, timing, and formulations of antioxidants, aiming to delineate strategies for their integration into prenatal care. In conclusion, this review provides insights into the promising role of antioxidants as therapeutic strategies to alleviate pregnancy complications associated with oxidative stress. It highlights avenues for future research, advocating for a deeper understanding of antioxidant mechanisms and their optimal utilization in prenatal care to enhance maternal and fetal health outcomes.

Background: Effective medication to manage diabetes mellitus-related organ complications with minimal adverse drug toxicity is still in pursuit by scientists worldwide. This study investigated the cardio-protective of Rida herbal bitter (RHB) in a high-fat diet/streptozotocin (STZ)-induced diabetic rats.Methods: Thirty-two matured male Wistar rats (250 ± 20g) were used. The animals were fed with high-fat diet (HFD) for 6 weeks before diabetes induction. A single dose of (35 mg/kgb.wt) freshly prepared STZ was injected intraperitoneally to induce diabetes. The animals were allocated into four groups, 8rats/group. Group I: control; Group II: HFD/STZ-induced diabetic rats; Groups III & IV: HFD/STZ-induced diabetic rats treated with 0.3 ml RHB & 200 mg/kgb.wt metformin respectively. At the end of the experiment, the animals were sacrificed, blood was sample collected via cardiac puncture and the heart was excised and homogenized. The blood samples and cardiac homogenates tissue were centrifuged to retrieve clear supernatant plasma for biochemical assay.Results: Diabetic rats exhibited significant (p < 0.05) elevated blood glucose, insulin, glycated hemoglobin (HbA1c), cardiac biomarkers, lipid profile, malondialdehyde (MDA), pro-inflammatory cytokines, food, and water intake levels with a reduction in body weight, cardiac antioxidant activity, and total protein. RHB administration significantly (p < 0.05) diminished the blood glucose, insulin, HbA1c, cardiac biomarkers, MDA, pro-inflammatory cytokines, lipid profile, food, and water intake, and improved the body weight cardiac antioxidant activity, and total protein.Conclusion: Rida herbal bitter possesses a cardio-protective effect from this study and could be a better alternative medication for managing diabetes and its related cardiovascular complications.

Background: The unwanted adverse toxicity displayed by synthetic antidiabetic medicine leads to the search for effective natural medicine to combat diabetes complications. This study investigated the cardioprotective of Anacardium occidentale nuts methanolic in high-fat diet (HFD)/streptozotocin (STZ)-induced diabetic rats.Materials and methods: Forty male adult Wistar were used and fed with HFD for 6 weeks before diabetes induction. The rats were grouped into 5 groups, 8 rats/group. Group I: normal control; Group II: diabetic control; Group III & IV: diabetic rats + 100 mg/kgb.wt & 200 mg/kgb.wt Anacardium occidentale nuts methanolic extract; Group V: diabetic rats + 200 mg/kgb.wt metformin. The rats were sacrificed on the experiment’s last day, blood samples were collected and the hearts were isolated for biochemical parameters estimation.Results: Food intake, water intake, plasmas insulin, Fasting Blood Glucose (FBG), glycosylated hemoglobin (HbA1c), cardiac enzymes, lipid profile, inflammatory cytokines, malondialdehyde, fibrotic marker, caspase-3 in cardiac of diabetic rats were elevated (p < 0.05) significantly. Body weight, cardiac antioxidant, and anti-apoptotic marker levels diminished (p < 0.05) significantly in diabetic rats. 100 mg/kgb.wt & 200 mg/kgb.wt of Anacardium occidentale nuts methanolic extract administration significantly suppressed the plasma insulin, FBG, HbA1c, cardiac lipid profile, cardiac enzymes biomarker, cardiac inflammatory cytokines, cardiac malondialdehyde, cardiac fibrotic marker, cardiac caspase-3, food intake & water intake and increased the body weight, cardiac antioxidant & cardiac anti-apoptotic marker in the diabetic rats.Conclusion: Anacardium occidentale nuts attenuate cardiac injury in diabetes. It could be a natural medicine to manage diabetes-cardiovascular complications.

The N-hydroxydodecanamide (HA12) and its complexes tri-hydroxamato-iron(III) and di-hydroxamto-iron(III) chloride (HA8Fe3 and HA12Fe3Cl, respectively) showed antibacterial and antimycobacterial activities. The proteomic analysis demonstrated that the targets of Hydroxamic Acid (HA) and their complexes were involved in the biosynthesis of mycobacterial cell walls. The Reactive Oxygen Species (ROS) is one of the key elements to cause oxidative stress, damaging DNA, and cell membranes impaired during the procedure to kill bacteria. Here, the ROS production was determined to evaluate the compounds HA12, HA8Fe3, HA12Fe3Cl, and ZnCl2 against bacteria using 2’,7’-dichlorofluorescein diacetate (DCFDA) by spectrofluorometric analysis. The low fluorescence was observed using the compounds HA12, HA8Fe3, HA12Fe3Cl, and ZnCl2 treating the S. aureus and E. coli, indicating that the ROS production could not be observed using the compounds used at a dose higher than the Minimum Inhibitory Concentration (MIC). It was noted that the ROS determination could be performed with a concentration less than or equal to the MIC. This would enable the mechanism of action linked to the ROS production by HA and their metal complexes to be determined.

Background: Linagliptin is an anti-diabetic drug that claims no adverse effects and treatment of gestational diabetes mellitus (GDM) demands a safe anti-diabetic medication. Therefore, this study investigates the anti-diabetic efficacy of linagliptin in an induced GDM.Materials and methods: Thirty-two matured female rats (100 - 200 g) were utilized. Sixteen non-pregnant/diabetic animals were fed with a normal diet and sixteen rats were fed with a high-fat (HFD), mated at the estrous stage in 2:1, and pregnancy was confirmed with a spermatozoa in a vaginal smear. The pregnant rats were intraperitoneally injected with a single dose (30 mg/kgb. wt)of streptozotocin (STZ) to induce GDM. The animals were grouped into 4 groups, 8 rats/groups. Group I: control; Group II: control + 10 mg/kgb.wt linagliptin; Group III: GDM; Group IV: GDM + 10 mg/kgb.wt linagliptin. The animals were sacrificed after 14 days of treatment. Blood samples were collected for biochemical parameters.Results: Fasting blood glucose (FBG) insulin, glycated hemoglobin (HbA1c), total cholesterol (TC), triglyceride (TG), low-density lipoprotein-cholesterol (LDL-C), malondialdehyde (MDA), interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-alpha (TNF-α) levels significant (p < 0.05) elevated in GDM rats, with significant reduction in high-density lipoprotein-cholesterol (HDL-C), catalase (CAT), superoxide dismutase (SOD) and reduced glutathione (GSH). Linagliptin administration significantly (p < 0.05) decreased the FBG, insulin, HbA1c, TC, TG, LDL-C, MDA, IL-6, IL-1β, and TNF-α and ameliorates the HDL-C, CAT, SOD, and GSH levels significantly.Conclusion: Linagliptin remarkably showed anti-hyperglycemic, anti-oxidative, and anti-inflammatory properties. Linagliptin could be a promising drug for hyperglycemia treatment during gestation.

Background: The impact of COVID-19 and long-term COVID-19 on gastrointestinal neoplasms remains underexplored. The current review investigates the potential link between these conditions and the role of gut microbiota in mediating oncogenic processes. Dysbiosis, characterized by alterations in gut microbial composition, may exacerbate inflammation and immune dysregulation, contributing to cancer development.Methods: A comprehensive literature review was conducted using databases including PubMed, Scopus, Embase, SciELO, and Web of Science. Inclusion criteria encompassed studies published between 2020 and 2024 that explored the intersection of COVID-19, long-term COVID-19, and gastrointestinal cancers. The articles were critically appraised for quality and relevance, and data were synthesized to elucidate common mechanisms and outcomes.Results: The review identifies several mechanisms by which gut microbiota may influence cancer risk in COVID-19 patients. Persistent inflammation, oxidative stress, and immune dysfunction observed in Long COVID were associated with dysbiosis. Specific microbial metabolites, such as secondary bile and short-chain fatty acids, were implicated in promoting tumorigenesis. Comparative analysis of studies suggests that SARS-CoV-2-induced dysbiosis may heighten susceptibility to gastrointestinal cancers, particularly in patients with prolonged post-infection symptoms.Conclusion: The findings underscore the need for further research to clarify the role of gut microbiota in cancer development among COVID-19 patients. These mechanisms could inform preventative strategies and therapeutic interventions, particularly for those experiencing COVID. The review highlights gaps in current knowledge and advocates for longitudinal studies to assess the long-term effects of COVID-19 on gastrointestinal health.

Treatment for HIV-associated neurocognitive disorders (HAND) remains elusive. 7,8-dihydroxyflavone (DHF), an analog of brain-derived neurotrophic factor (BDNF) and a high-affinity TrkB agonist, has been proposed as a viable therapeutic alternative to BDNF in crossing the Blood-Brain Barrier (BBB) and promoting growth, differentiation, maintenance, and survival of neurons. Here, we expand on our previous study investigating the therapeutic role of DHF on the cortical and hippocampal brain regions of the Tg26 mice, an animal model of HAND. We detected increased immunoreactivity for ion channels (SUR1, TRPM4) and the water channel aquaporin-4 (AQP4), suggesting an ionic and osmotic imbalance in the brains of Tg26 mice. Tg26 mice also exhibited loss of synaptic stability (SYN, SYP) and nicotinamide metabolism (NAMPT, SIRT1) that were associated with astrogliosis. Furthermore, Tg26 mice demonstrated increased iNOS and reduced HO-1/NRF2 expressions, implicating increased ER and oxidative stress. DHF treatment in Tg26 mice reversed these pathological changes. These data suggest crosstalk among TrkB, Akt, and related transcription factors (NF-κB, STAT3, and NRF2) as an underlying mechanism of Tg26-associated pathology in the brain. Finally, taken together with our prior study, these results further highlight a therapeutic role of DHF in promoting neuroprotection in HAND that may be applied in conjunction with current antiviral therapies.

In the world, millions of hectares of cultivated land are affected by salt, making salinity a major constraint for plant production. The effects of different levels of banana peel on growth, yield, and chemical changes of jute (Corchorus olitorius L.) under salt stress were examined herein. Response of jute to applications of different levels of banana peel (5, 10, and 15 t ha-1), as well as water irrigation salinity at 50, 100, and 200 mM NaCl were evaluated under greenhouse conditions. The outcome uncovered that salinity caused significant reduction of plant growth and yield parameters, chlorophyll (at 21.6%), LRWC (at 18.9%), P (at 57.1%) and K (at 45.4%) content, while MDA content (at 351.8%), Na (at 266%), soluble proteins (70.2%), total phenolic (at 23.4%) accumulation showed an increase from 0 to 200 mM NaCl without BP application. The banana peel treatments (at 15 t ha-1 under 200 mM NaCl) diminished significantly damaging effects caused by salinity via a reduction in the Na (at 28.4%), total soluble sugars (at 17.8%), total flavonoids (at 20.1%), which enhanced number of leaves per plant (37.1%), plant height (at 19.8%), leave yield (at 41.4%), LRWC (at 12.8%), Mg (at 24.2%) and reduced the MDA content (at 20%), presenting a favorable effect in reducing the oxidative stress that emerged from salt stress. It could be concluded, that the application of 15 t ha-1 of BP was superior in promoting plant growth, yield, and nutritional quality than others under control and in the saline soils in this study. BP at 15 t ha-1 had a more reduced damage of salt stress effect on growth, yield, nutritional value, and use efficiency.

Stroke and acute myocardial infarction are primary global causes of mortality. Statistical studies have shown that acute myocardial infarction is responsible for around 9 million deaths each year. Ischemic stroke and myocardial infarction have a significant role in global adult physical disabilities. While reperfusion is vital for tissue recovery, it may paradoxically, inadvertently increase damage through oxidative stress, inflammation, and cell death. Early reperfusion procedures are currently the sole therapy to reduce infarct size. There are many mysteries about heart biology. It is not known the source of energy for myocardial tissues. The heart-beating force (120 mm Hg) cannot explain how erythrocytes are impelled through almost 95,000 km of capillaries in less than 5 minutes. A better knowledge of how the heart is oxygenated should allow the development of new therapies.

Methylenetetrahydrofolate Reductase (MTHFR) is an important enzyme of the folate cycle, which is required to convert 5,10-methyltetrahydrofolate into 5-methyltetrahydrofolate (5-methylTHHF). 5-methyl THF is a methyl group donor for several cellular methylation processes. It also donates methyl group for the conversion of homocysteine into methionine, the higher concentration of which is toxic. MTHFR gene C677T polymorphism is clinically important polymorphism and the variant MTHFR (A222V) enzyme has reduced activity, hence increasing the requirement for folic acid. Less conversion of folate to 5-methyl-THF due to C677T polymorphism results in a higher plasma concentration of homocysteine (hyperhomocysteinemia). Individuals having C677T polymorphism are susceptible to various diseases, including reproductive problems like male infertility, polycystic ovary syndrome, Recurrent Pregnancy Loss (RPL), Preeclampsia (PE), placental abruption, and adverse pregnancy outcomes. MTHFR C677T polymorphism mimics folate deficiency, and folate is required for DNA synthesis, repair, methylation, and proper chromosome segregation, and all these processes are important for foetal growth and normal development. Methylation and demethylation processes control the gene expression of about 45% of human genes. Impaired methylation influences the expression of genes involved in the regulation of hormones, spermatogenesis, and oogenesis. In males, oxidative stress damages sperm DNA decreases sperm motility, and may impair fertilization capability. In pregnant women, hyperhomocysteinemia increases oxidative stress and inflammation within the placenta, which causes damage to placental tissue, impairs its function, and disrupts foetal development. Further, hyperhomocysteinemia (HHcy) is embryotoxic and neurotoxic and is responsible for congenital anomalies in the foetus. This review supports the idea that MTHFR C677T polymorphism is associated with an increased risk for male infertility, PCOS, RPL, PE, and congenital anomalies. This review may provide a clue toward a better understanding of the correlation between the MTHFR C677T polymorphism and its detrimental effects on human reproductive health.