Serum Oxidative Stress Research Articles

Effects of non-invasive vagus nerve stimulation on clinical symptoms and molecular biomarkers in Parkinson's disease.

Non-invasive vagus nerve stimulation (nVNS) is an established neurostimulation therapy used in the treatment of epilepsy, migraine and cluster headache. In this randomized, double-blind, sham-controlled trial we explored the role of nVNS in the treatment of gait and other motor symptoms in Parkinson's disease (PD) patients. In a subgroup of patients, we measured selected neurotrophins, inflammatory markers and markers of oxidative stress in serum. Thirty-three PD patients with freezing of gait (FOG) were randomized to either active nVNS or sham nVNS. After baseline assessments, patients were instructed to deliver six 2 min stimulations (12 min/day) of the active nVNS/sham nVNS device for 1 month at home. Patients were then re-assessed. After a one-month washout period, they were allocated to the alternate treatment arm and the same process was followed. Significant improvements in key gait parameters (speed, stance time and step length) were observed with active nVNS. While serum tumor necrosis factor- α decreased, glutathione and brain-derived neurotrophic factor levels increased significantly (p < 0.05) after active nVNS treatment. Here we present the first evidence of the efficacy and safety of nVNS in the treatment of gait in PD patients, and propose that nVNS can be used as an adjunctive therapy in the management of PD patients, especially those suffering from FOG. Clinical trial registration: identifier ISRCTN14797144.

Evaluation of antioxidant system and oxidative stress in serum of pregnant women with physiological pregnancy and fetal growth restriction

Evaluation of antioxidant system and oxidative stress in serum of pregnant women with physiological pregnancy and fetal growth restriction

Abstract TMP114: The Role of Iron Mediated Oxidative Stress and Lipid Peroxidation in the Development of Intracranial Aneurysm Rupture

Introduction: Iron is an essential element for vascular wall maintenance. However, iron deposition in the vascular wall may cause oxidative stress, which can attack DNA, proteins, and lipid membranes via the Fenton/Haber-Weiss reaction. Iron-induced oxidative stress triggers lipid oxidation, inflammation, endothelial cell activation and intracranial aneurysmal formation, growth, and rupture. Subarachnoid hemorrhage from intracranial aneurysm rupture results in significant morbidity and mortality. This study used a mouse model of intracranial aneurysm to evaluate the effect of dietary iron restriction on aneurysm formation and rupture. Methods: Intracranial aneurysms were induced using deoxycorticosterone acetate-salt-induced hypertension and a single injection of elastase into the cerebrospinal fluid of the basal cistern. Mice were fed an iron-restricted diet or a normal diet. Aneurysm rupture was detected by neurological symptoms, while the presence of intracranial aneurysm with subarachnoid hemorrhage was confirmed by post-mortem examination. Results: The aneurysmal rupture rate was significantly lower in iron-restricted diet mice (37%) compared with normal diet mice (76%; p &lt; 0.05). Serum oxidative stress, iron accumulation, macrophage infiltration, and 8-hydroxy-2′-deoxyguanosine in the vascular wall were lower in iron-restricted diet mice ( p &lt; 0.01). The areas of iron positivity were similar to the areas of CD68 positivity and 8-hydroxy-2′-deoxyguanosine in both normal diet and iron-restricted diet mice aneurysms. Conclusions: Compared with a normal diet, an iron-restricted diet reduced the incidence of intracranial aneurysmal rupture in mice via inhibition of iron accumulation in the aneurysmal wall. Iron may be a potential therapeutic target to prevent intracranial aneurysm rupture. Long-term iron restriction may be required to affect aneurysm formationrupture.

Therapeutic effects of Medicago sativa against cyclophosphamide-induced toxicity in rats.

Medicago sativa (M. sativa) has been traditionally used for treating anemia; therefore, M. sativa hydro-ethanolic extract therapeutic effects against cyclophosphamide (CP) -induced hematologic and liver toxicity were examined. Thirty male Wistar rats were randomly divided to control (saline); CP (100 mg/kg, day 1-3, subcutaneously); CP+ M. sativa 200 mg/kg (MS 200); CP+ M. sativa 400 mg/kg (MS 400); CP+ dexamethasone (0.1 mg/kg), (all groups n=6). Treated animals received M. sativa or dexamethasone by gavage from days 7-14. On days 0, 7, and 14, hematologic parameters, and on the 14th day, serum and liver tissue oxidative stress markers including nitric oxide, malondialdehyde (MDA) and total thiol levels, superoxide dismutase (SOD) and catalase (CAT) activities, serum lipids, and liver enzymes were measured. Animal weight, platelet, white blood cells, and red blood cells counts, hemoglobin and hematocrit as well as thiol, SOD, and CAT activities in serum and liver tissue were significantly reduced, but serum nitric oxide, MDA, total cholesterol, triglycerides, low-density lipoproteins levels, and liver enzymes were increased in the CP group compared to the control group (p<0.05 to p<0.001). Administering M. sativa extract (400 mg/kg) significantly enhanced platelet count, and SOD and CAT activities and inhibited all of the CP toxic effects, while dexamethasone improved platelet count and oxidative stress markers compared to the CP group (p<0.05 to p<0.001). The extract of M. sativa (400 mg/kg) showed therapeutic effects against the CP-induced myelosuppression and thrombocytopenia and improved oxidative stress markers which were comparable to the effect of dexamethasone.

Serum Oxidative Stress Biomarkers and their correlation with severity of Obstructive Sleep Apnea - A Cross Sectional Study

Serum Oxidative Stress Biomarkers and their correlation with severity of Obstructive Sleep Apnea - A Cross Sectional Study

The effects of hydrolyzed protein on macronutrient digestibility, fecal metabolites and microbiota, oxidative stress and inflammatory biomarkers, and skin and coat quality in adult dogs.

Research on protein hydrolysates has observed various properties and functionalities on ingredients depending on the type of hydrolysate. The objective of this study was to evaluate the effects of hydrolyzed chicken protein that was incorporated into diets on digestibility, gut health, skin and coat health, oxidative stress, and intestinal inflammation markers in healthy adult dogs. Five complete and balanced diets were manufactured: (1) CONd: 25% chicken meal diet; (2) 5% CLHd: 5% chicken liver and heart hydrolysate plus 20% chicken meal diet; (3) CLHd: 25% chicken liver and heart hydrolysate diet; (4) 5% CHd: 5% chicken hydrolysate plus 20% chicken meal diet; (5) CHd: 25% chicken hydrolysate diet. A replicated 5 × 5 Latin square design was used which included 10 neutered adult Beagles. Each of the 5 periods consisted of a 7-d washout time and a 28-d treatment period. All diets were well accepted by the dogs. Fecal butyrate concentration was higher while fecal isovalerate and total phenol/indole were lower in dogs fed CLHd than CONd (P < 0.05). Dogs fed CHd had higher fecal immunoglobulin A concentration when compared with CLHd (P < 0.05); however, both groups were comparable to the CONd. There was no difference among groups in serum cytokine concentrations, serum oxidative stress biomarkers, or skin and coat health analyses (P > 0.05). Fecal microbiota was shifted by CLHd with higher abundance in Ruminococcus gauvreauii group as well as lower Clostridium sensu stricto 1, Sutterella, Fusobacterium, and Bacteroides when compared with CONd (P < 0.05). There was also a difference in beta diversity of fecal microbiota between CLHd and CHd (P < 0.05). In conclusion, chicken protein hydrolysate could be incorporated into canine extruded diets as a comparable source of protein to traditional chicken meal. The test chicken protein hydrolysates showed the potential to support gut health by modulating immune response and microbiota; however, functional properties of protein hydrolysates are dependent on inclusion level and source.

Protective effects of Tinospora cordifolia miers extract against hepatic and neurobehavioral deficits in thioacetamide-induced hepatic encephalopathy in rats via modulating hyperammonemia and glial cell activation

Ethnopharmacological relevanceTinospora cordifolia (TC) a potential medicinal herb, has been ethnobotanically used as an eco-friendly supplement to manage various diseases, including cerebral fever. Earlier studies have shown that TC exhibits diverse beneficial effects, including hepatoprotective and neuroprotective effects. However, the effects of TC remain unexplored in animal models of encephalopathy including hepatic encephalopathy (HE). Aim of the studyTo evaluate the effects of TC stem extract against thioacetamide (TAA)-induced behavioural and molecular alterations in HE rats. Methods and materialsThe extract was preliminarily screened through phytochemical and HR-LC/MS analysis. Animals were pre-treated with TC extract at doses 30 and 100 mg/kg, orally. Following 7 days of TC pre-treatment, HE was induced by administering TAA (300 mg/kg, i. p. thrice). Behavioural assessments were performed after 56 h of TAA first dose. The animals were then sacrificed to assess biochemical parameters in serum, liver and brain. Liver tissue was used for immunoblotting and histological studies to evaluate inflammatory and fibrotic signalling. Moreover, brain tissue was used to evaluate brain edema, activation of glial cells (GFAP, IBA-1) and NF-κB/NLRP3 downstream signalling via immunoblotting and immunohistochemical analysis in cortex and hippocampus. ResultsThe pre-treatment with TC extract effective mitigated TAA-induced behavioural alterations, lowered serum LFT (AST, ALT, ALP, bilirubin) and oxidative stress markers in liver and brain. TC treatment significantly modulated hyperammonemia, cerebral edema and preserved the integrity of BBB proteins in HE animals. TC treatment attenuated TAA-induced histological changes, tissue inflammation (pNF-κB (p65), TNF-α, NLRP3) and fibrosis (collagen, α-SMA) in liver. In addition, immunoblotting analysis revealed TC pre-treatment inhibited fibrotic proteins such as vimentin, TGF-β1 and pSmad2/3 in the liver. Our study further showed that TC treatment downregulated the expression of MAPK/NF-κB inflammatory signalling, as well as GFAP and IBA-1 (glial cell markers) in cortex and hippocampus of TAA-intoxicated rats. Additionally, TC-treated animals exhibited reduced expression of caspase3/9 and BAX induced by TAA. ConclusionThis study revealed promising insights on the protective effects of TC against HE. The findings clearly demonstrated that the significant inhibition of MAPK/NF-κB signalling and glial cell activation could be responsible for the observed beneficial effects of TC in TAA-induced HE rats.

The efficacy of Makiang tea drinking on serum lipid profile in the treatment of dyslipidaemia: A randomized controlled trial

The purpose of this study was to investigate the effects of Makiang (MK) tea consumption on the serum lipid profile and oxidative stress biomarkers in participants with dyslipidemia. A randomized, single-blind, parallel-group, placebo-controlled study was conducted at the Outpatient Department of Phayao Hospital, Thailand. This clinical trial enrolled 64 subjects (males and females), aged between 30 and 65 years with hyperlipidemia who were randomized using simple random sampling, receiving a 12-week MK tea (3 g/250 ml hot water) taken daily or a placebo. Body mass index, lipid profile, and serum oxidative stress markers were evaluated at the baseline and the end of the study. Within-group comparisons revealed that drinking only one cup of MK tea daily caused a significant reduction (p &lt; 0.05 all) of total cholesterol (TC), total triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C). Meanwhile, between-group differences showed that serum TC, TG, and LDL-C levels significantly decreased (p &lt; 0.05 all), whereas the levels of high-density lipoprotein cholesterol were unchanged. This phenomenon was accompanied by decreased serum malondialdehyde and increased endogenous enzymatic defence systems (p &lt; 0.05 all). Thus, MK tea may be useful as an adjunct agent to improve the lipid profile in patients with dyslipidemia.

Eugenol Improved Antioxidant Status, Proinflammatory and Apoptotic Markers on Rats Exposed to Cardiotoxicity

The current study was conducted to evaluate the cardioprotective potentials of eugenol against hypertension induced by doxorubicin in rats. Rats were exposed to Doxorubicin HCl (2mg/kg body weight) intraperitoneally to induce cardiotoxicity and treated with eugenol (5 mg/kg) orally for 5 weeks. At the end of the study, the blood pressure was assessed in the tested animals and the levels of serum lipid profile and oxidative stress markers were assessed. Also, the heart was dissected and the oxidative stress and apoptotic markers in heart homogenate were assessed. There was high statistically significant difference between all the tested groups regarding the systolic blood pressure and mean arterial pressure. The Serum oxidative stress markers and lipid profile markers showed a statistically significant increase in the positive control group compared to other groups. The heart homogenate level of all the tested parameters showed a statistically significant increase in the positive group compared to other groups except for the MDA levels that was comparable between the positive group and protection group. Eugenol's antioxidant and lipid-lowering properties protect against hypertension. Eugenol's antioxidant and anti-apoptotic effects protect the heart from hypertension's long-term effects at the tissue level.

Influence of omega- 3 fatty acids, soya isoflavones and their combination for abrogating carbon tetrachloride hazards in male rats.

Studies have shown that carbon tetrachloride (CCl4) induces hepatic and renal damage arising from oxidative stress. The present study was undertaken to examine the effect of omega-3 fatty acids and/or soya isoflavones on CCl4 induced toxicity in male albino rat liver and kidney. For this purpose, 42 rats were divided as follows: group 1, rats serves as the control without any treatment; group 2, rats were administered a single dose of CCl4 intraperitoneally (1 mg/kg b. wt.); group 3, rats were supplemented daily with omega-300 orally (400 mg/kg b. wt.); group 4, rats were supplemented daily with pro-S orally (50 mg/kg b. wt.); group 5, rats were supplemented daily with omega-300 orally for four weeks, then after 24 hours treated with a single dose of CCl4 at the same tested doses. group 6, rats were supplemented daily with pro- S orally for four weeks, then after 24 hours treated with a single dose of CCl4 at the same tested doses; group 7, rats were supplemented daily with an oral combination of omega-300 and pro-S orally for four weeks, then after 24 hours treated with a single dose of CCl4 at the same tested doses. Results showed that CCl4 administration induces hepatic damage indicated by a significant increase in the activities of alkaline phosphatase (ALP), aspartate aminotransferase (AST) and Aalanine aminotransferase (ALT) enzymes and glucose level, with a significant increase in malondialdehyde (MDA) and nitric oxide (NO) levels and a significant decrease of reduced glutathione (GSH) level in liver tissue. Also, CCl4 toxicity induce renal damage manifested in a significant increase in serum urea, creatinine, uric acid, and oxidative stress of kidney tissue reflected by increase of MDA, NO and the decrease of GSH levels. The pre-treatment with omega-3 fatty acids and/or soya isoflavones revealed ameliorative effect against deleterious effects of CCl4 toxicity on hepatic and renal tissues and all tested parameters. Results of the current study revealed also that the pre-treatment with omega-3 fatty acids and/or soya isoflavones to rats improved liver and kidney function and produced high antioxidant activity.

Comparison of the hepatoprotection of intragastric and intravenous cyanidin-3-glucoside administration: focus on the key metabolites and gut microbiota modulation.

Liver injury is a life-threatening condition, and the hepatoprotective potential of cyanidin-3-glucoside (C3G) has been previously demonstrated. However, due to the low bioavailability, it has been doubtful that relatively low concentrations of intact C3G in vivo could account for these bioactivities. In this study, the hepatoprotective effects of intragastric and intravenous administration of C3G were investigated in a CCl4 induced liver injury model. Intragastric C3G administration was more effective than intravenous C3G injection in reducing serum damage biomarkers, oxidative stress, and inflammatory responses, indicating that absorption of C3G into the bloodstream does not fully account for its observed benefits in vivo. Furthermore, intragastric C3G administration modulated the gut microbiota structure and increased the contents of five metabolites in the feces and serum with high inter-individual variation, indicating the key role of the interaction between C3G and the gut microbiota. At equivalent doses, the metabolites cyanidin and protocatechuic acid exhibited greater efficacy than C3G in reducing apoptosis and ROS production by activating the Nrf2 pathway in an AAPH-induced oxidative stress model. To achieve the desired health effects via C3G-rich food intake, more attention should be paid to microbially derived catabolites. Screening of specific metabolite-producing strains will help overcome individual differences and enhance the health-promoting effects of C3G.

Biological Markers in Newly Diagnosed Generalized Anxiety Disorder Patients: 8-OHdG, S100B and Oxidative Stress.

Generalized Anxiety Disorder (GAD) is a chronic disease persisting for at least 6 months, characterized by excessive and continuous anxiety, which leads to evident problems and functional disorders. S100B is a glial protein that plays a role in intercellular communication regulating cell growth and differentiation, and intracellular signal transmission. This study aimed to analyze the serum S100B, 8-OHdG, and oxidative stress levels of patients newly diagnosed with GAD who had not started treatment, to better understand the underlying neurobiological basis of the etiology of GAD. Forty-four patients diagnosed with GAD according to DSM-5 diagnostic criteria and 44 healthy controls were included in the study. The Beck Anxiety Inventory (BAI) was used to determine the anxiety levels of the GAD patients. The serum S100B, 8-OHdG, total oxidant status (TOS), and total antioxidant status (TAS) levels were measured in the patient and control groups. The 8-OHdG values of the GAD group were determined to be statistically significantly higher than those of the control group (p=0.028). No significant difference was determined between the GAD patients and the control group in respect of the TAS, TOS, and oxidative stress index (OSI) values (p>0.05). The S100B levels of the GAD group were found to be higher than those of the control group. The results of this study showed that there could be DNA damage because of oxidative stress in GAD patients. There is a need for further studies to confirm the role of S100B protein in GAD etiology and pathogenesis.

Anti-inflammatory and anti-oxidant action of tadalafil in testicular regeneration process after heat stress.

Tadalafil, a potent phosphodiesterase inhibitor 5 (PDE-5), is commonly used for the management of erectile dysfunction. However, its therapeutic potential extends beyond this indication. This study aimed to investigate the impact of tadalafil on the recovery of testicular parenchyma in male Wistar rats exposed to testicular thermal stress. Fifty-four Wistar rats were subjected to testicular thermal stress and randomly assigned to receive either tadalafil treatment (TAD) or no treatment (control). TAD was administered intraperitoneally at a dose of either 0.9 mg/kg or 1.8 mg/kg. Biometric parameters, histopathological assessment of the testis, serum testosterone levels, oxidative stress, and interleukin levels were evaluated on days 7, 15, and 30 after thermal shock. The animals were euthanized at the end of each experimental period, and samples were collected. TAD treatment maintained testicular weight and reduced the testicular degenerative process up to day 7 post-injury. However, despite TAD therapy, serum testosterone levels were decreased in the treated groups at days 7 and 15 post-thermal stress. TAD also decreased TNF-α and NO levels at different doses but had no effect on IL-6. The treatment with TAD after heat shock demonstrated anti-inflammatory and antioxidant properties but did not prevent the aggravation of testicular lesions in subsequent periods, even with the systematic reduction in TNF-α and NO levels. Therefore, this selective PDE-5 inhibitor, at the dosages used, did not have a positive impact on testosterone levels during the post-thermal stress period, which could compromise the resumption of the spermatogenic process.

Polyherbal extract improves glycometabolic control in alloxan-induced diabetic rats via down-regulating the MAPK/JNK pathway, modulating Nrf-2/Keap-1 expression, and stimulating insulin signaling.

This study focused on the evaluation of antioxidant and antidiabetic activities of polyherbal extract (PHE), containing Cassia absus (L.), Gymnema sylvestre (R. Br.), Nigella sativa (L.), and Piper nigrum (L.), in alloxan-induced diabetes model. In vitro, HPLC characterization, DPPH scavenging assay, and α-amylase inhibition test were conducted. In vivo, acute oral toxicity of PHE was assessed. Alloxan-induced diabetic Wistar rats (n=6) were orally treated with PHE (200, 400, and 600 mg/kg/day) and glibenclamide (GLB; 10 mg/kg/day) for six consecutive weeks. Then, biochemical biomarkers, oxidative stress parameters, histopathological examination, and mRNA expression levels (RT-qPCR) were determined. The presence of polyphenols in PHE was confirmed in correlation to marked DPPH scavenging (IC50: 1.60 mg/ml) and α-amylase inhibition (IC50: 0.82 mg/ml). PHE demonstrated no toxicity in rats up to a dose of 2000 mg/kg. In diabetic rats, PHE dose-dependently ameliorated the serum levels of glucose, insulin, glycated hemoglobin A1c (HbA1c), leptin, and glucokinase (GCK). Also, PHE substantially alleviated serum inflammatory markers (TNF-α and CRP) and oxidative stress indicators (MDA, SOD, and CAT) in pancreatic tissues. PHE, particularly at 600 mg/kg, attenuated cellular oxidative stress via modulating the mRNA expression levels of genes regulating MAPK/JNK (Mapk-8, Traf-4, and Traf-6) and Nrf-2/Keap-1 pathways and promoted insulin signaling through up-regulating insulin signaling cascade (Pdx-1, Ins-1, and Ins-2), as compared to GLB. Furthermore, histopathological findings supported the aforementioned results. Our study suggests that polyherbal extract has promising antioxidant and antidiabetic activities by modulating the MAPK/JNK, Nrf-2/Keap-1, and insulin signaling pathways.

Bacillus halotolerans attenuates inflammation induced by enterotoxigenic Escherichia coli infection in vivo and in vitro based on its metabolite soyasaponin I regulating the p105-Tpl2-ERK pathway.

Soyasaponins, recognized for their anti-inflammatory and antioxidant effects, have not yet been fully explored for their role in combating enterotoxigenic Escherichia coli (ETEC) infections. Recent findings identified them in small-molecule metabolites of Bacillus, suggesting their broader biological relevance. This research screened 88 strains of B. halotolerans, identifying the strain BH M20221856 as significantly inhibitory against ETEC growth in vitro. It also reduced cellular damage and inflammatory response in IPEC-J2 cells. The antimicrobial activity of BH M20221856 was attributed to its small-molecule metabolites rather than secretory proteins. A total of 69 small molecules were identified from the metabolites of BH M20221856 using liquid chromatography mass spectrometry/mass spectrometry (LC-MS/MS). Among these, soyasaponin I (SoSa I) represented the largest multiple change in the enrichment analysis of differential metabolites and exhibited potent anti-ETEC effects in vivo. It significantly reduced the bacterial load of E. coli in mouse intestines, decreased serum endotoxin, D-lactic acid, and oxidative stress levels and alleviated intestinal pathological damage and inflammation. SoSa I enhanced immune regulation by mediating the p105-Tpl2-ERK signaling pathway. Further evaluations using transepithelial electrical resistance (TEER) and cell permeability assays showed that SoSa I alleviated ETEC-induced damage to epithelial barrier function. These results suggest that BH M20221856 and SoSa I may serve as preventative biologics against ETEC infections, providing new insights for developing strategies to prevent and control this disease.

Relationship between serum AGE precursor levels, oxidative stress, and quality of life in patients receiving hemodialysis

Introduction/Objective. The aim of this study was to determine the relationship between serum advanced glycation end product (AGE) precursors, oxidative stress levels, and quality of life in hemodialysis patients. Methods. A descriptive form and the Kidney Disease Quality of Life Form (KDQOL-36) were used in the study. Serum levels of AGE precursors [methylglyoxal (MGO) and glyoxal (GO)] and oxidative stress [malondialdehyde (MDA)] were determined in blood samples taken from the patients. Results. The KDQOL-36 subscale scores were 71.65 ? 17.76 for the symptoms/problems list, 66.35 ? 19.06 for the effect of kidney disease, 40.6 ? 24.01 for the kidney disease burden, 41.6 ? 9.83 SF-12 for physical health, and 37.83 ? 9.69 for SF-12 mental health. The serum levels were 3.96 ? 1.01 ?mol/L for MDA, 1029.87 ? 314.43 ng/mL for GO, and 115.2 ? 75.54 ng/mL for MGO. A positive and significant correlation was detected between serum MGO and GO (r = .285, p &lt; 0.01) and MDA (r = 0.284, p &lt; 0.01). A positive correlation was noted between serum MDA and GO (r = 1,000, p &lt; 0.05) and a negative correlation with kidney disease burden (r = -0.205, p &lt; 0.05). A negative and significant correlation was detected between GO and kidney disease burden (r = -0.204, p &lt; 0.05). Conclusion. Serum MGO, GO, and MDA levels were high in patients undergoing hemodialysis. High serum MDA levels are associated with high serum GO and MGO levels. High serum levels of MDA and GO had a negative impact on the quality of life of hemodialysis patients.

Effect of niclosamide ethanolamine on the serum oxidative stress markers in cardiac injury

Effect of niclosamide ethanolamine on the serum oxidative stress markers in cardiac injury

Assessment of Cerebral Hypoxemia and Its Impact on Cognitive and Psychological Functions in Patients With Obstructive Sleep Apnea Syndrome

Background and Objective The precise pathophysiology of cognitive impedance and mental illness in obstructive sleep apnea (OSA) patients remains elusive. Therefore, there is a need for studies on novel diagnoses and therapeutic strategies for cognitive impairment in OSA patients. This work aimed to evaluate cerebral hypoxemia, its consequences on brain metabolism, and local and systemic inflammation, and their subsequent impact on cognitive and psychological functioning.Methods This cross-sectional case-control study was conducted on 30 eligible OSA patients and 20 age/sex-matched healthy controls. All the participants underwent one-night polysomnography, and cognitive evaluation was done using the Mini-Mental State Examination, Montreal Cognitive Assessment, Brief Kingston Standardized Cognitive Assessment, D2 Test of Consideration (to evaluate attention problems), and Wisconsin card sorting test. The psychiatric assessment included the Arabic form of the Hamilton Depression Rating Scale and Beck Depression Inventory-II. A radiology assessment was done using proton magnetic resonance spectroscopy. Neurophysiological assessment was done using the potential cortical (N20) latency and amplitude of somatosensory evoked potential. Laboratory examinations included serum levels of NF-κB, HMGB1, and HIF-1α.Results Polysomnography demonstrated noteworthy increase in the apnea-hypopnea index, respiratory disturbance index, arousal index, snoring index, and wake after sleep onset. It also showed diminished sleep efficiency, total sleep time, and SaO2 nadir in the OSA group. Neuropsychological scales demonstrated poor performance in global cognitive tests, particular cognitive domains impedance, and depression in the OSA group, with noteworthy differences within the group. Magnetic resonance spectroscopy highlighted that OSA patients had a noteworthy bilateral decrement in N-acetylaspartate (NAA) peak, creatine peak, and NAA/choline proportion and an increment in choline peak, lipid peak, lactate peak, choline/creatine proportion, and NAA/creatine proportion in the frontal white matter, hippocampus, and parieto-occipital cortex. Moreover. OSA patients had either missing or decreased amplitude and delayed latency of N20. There was a noteworthy rise of serum inflammatory marker NF-κB, HMGB1, and oxidative stress marker HIF-1α in OSA patients.Conclusions Chronic intermittent hypoxia with resulting amplified inflammatory and oxidative stress in OSA patients may affect brain metabolism; consequently, leading to cognitive and psychological dysfunctions.

Evaluation of health risk associated with consumption of food crops from electronic waste dumpsite using albino Wistar rat’s model: Bayelsa state Nigeria case study

The alterations in some important health biomarkers associated with consumption of food crops harvested near E-waste dumpsite in Bayelsa State, Nigeria, was evaluated. Samples of soil, plant, water and sea foods were collected around E-waste dumpsites and control sites for laboratory screening. A standard animal feed was formulated (control group), and the feed formulated from plants harvested from e-waste dumpsites was used to feed the experimental animals (Test group) for a period of three months. The formulated feeds were screened for toxic metals using atomic absorption spectrometry. The study comprises of twenty-eight animals (fourteen each of male and female) of albino wistar strain, weighing 50-100g were divided into two groups of fourteen animals each. Health biomarkers such as C-reactive protein, TNF alpha, creatinine, alanine transaminase (ALT), aspartate transaminase (AST), alanine phosphatase (ALP), platelet count, and oxidative stress parameters were evaluated in both groups. Toxic metals content of samples collected from the E-waste dumpsite revealed significantly (p&lt;0.05) higher levels of Cd, Co, Ni and Pb, which exceeded WHO permissible limits, compared with the control (p&lt;0.05) site. Significant (p&lt;0.05) differences between the test and control group for serum C-reactive protein, TNF alpha, creatinine concentrations, ALT, AST, ALP activities, platelet count, and oxidative stress parameters of the test group were all significantly (p&lt;0.05) higher than the control group, suggesting the presence of oxidative stress trigger(s) among animals in the test group and these results were further affirmed by the histology results as presented. Conclusively, this study highlighted a strong correlation between consumption of food crops cultivated near E-wastes dumpsites and potential associated health risks. Hence, demands public awareness and a call on governments and concerned regulatory bodies to ensure and enforce ethical E-waste management and disposal practices to minimize E-waste exposure and toxicity.

Lactiplantibacillus plantarum NKK20 Increases Intestinal Butyrate Production and Inhibits Type 2 Diabetic Kidney Injury through PI3K/Akt Pathway.

Nephropathy injury is a prevalent complication observed in individuals with diabetes, serving as a prominent contributor to end-stage renal disease, and the advanced glycation products (AGEs) are important factors that induce kidney injury in patients with diabetes. Addressing this condition remains a challenging aspect in clinical practice. The aim of this study was to explore the effects of Lactiplantibacillus plantarum NKK20 strain (NKK20) which protects against diabetic kidney disease (DKD) based on animal and cell models. The results showed that the NKK20 can significantly reduce renal inflammatory response, serum oxidative stress response, and AGE concentration in diabetic mice. After treatment with NKK20, the kidney damage of diabetic mice was significantly improved, and more importantly, the concentration of butyrate, a specific anti-inflammatory metabolite of intestinal flora in the stool of diabetic mice, was significantly increased. In addition, nontargeted metabolomics analysis showed a significant difference between the metabolites in the mouse serum contents of the NKK20 administration group and those in the nephropathy injury group, in which a total of 24 different metabolites that were significantly affected by NKK20 were observed, and these metabolites were mainly involved in glycerophospholipid metabolism and arachidonic acid metabolism. Also, the administration of butyrate to human kidney- (HK-) 2 cells that were stimulated by AGEs resulted in a significant upregulation of ZO-1, Occludin, and E-cadherin gene expressions and downregulation of α-SMA gene expression. This means that butyrate can maintain the tight junction structure of HK-2 cells and inhibit fibrosis. Butyrate also significantly inhibited the activation of PI3K/Akt pathway. These results indicate that NKK20 can treat kidney injury in diabetic mice by reducing blood glucose and AGE concentration and increasing butyrate production in the intestine. By inhibiting PI3K pathway activation in HK-2 cells, butyrate maintains a tight junction structure of renal tubule epithelial cells and inhibits renal tissue fibrosis. These results suggest that NKK20 is helpful to prevent and treat the occurrence and aggravation of diabetic kidney injury.