Decrease In Antioxidant Status Research Articles

Tumor necrosis factor α1 decreases mucosal immune and antioxidant response in the midgut of hybrid fish (white crucian carp ♀ × red crucian carp ♂).

Tumor necrosis factor α1 (TNFα) is a pleiotropic cytokine involved in immune regulation and cellular homeostasis, but the crucial role of TNFα in fish gut remained unclear. The current study aimed to evaluate the immunoregulatory function of TNFα1 on gut barrier in a novel hybrid fish (WR), which was produced by crossing white crucian carp (Carassius cuvieri, ♀) with red crucian carp (Carassius auratus red var, ♂). In this study, WR-tnfα1 sequence was identified, and a high-level expression was detected in the intestine. Elevated levels of WR-tnfα1 expressions were detected in immune-related tissues and cultured fish cells on stimulation. The appearance of vacuolization and submucosal rupture was observed in TNFα1-treated midgut of WR, along with elevated levels of goblet cell atrophy, whereas no significant changes were detected in most expressions of tight-junction genes and mucin genes. In contrast, WR receiving gut perfusion with WR-TNFα1 showed a remarkable decrease in antioxidant status in midgut, whereas the expression levels of apoptotic genes and redox responsive genes increased sharply. These results suggested that TNFα1 could exhibit a detrimental effect on antioxidant defense and immune regulation in the midgut of WR.

Alcohol-induced hormonal and metabolic alterations in plasma and erythrocytes—a gender-based study

Purpose This study aimed to understand the gender-specific alcohol-induced biochemical changes and TBARS association with the endocrine system. Methods Human male and female subjects ranging from 35 ± 10 years old with an 8-10-year drinking history were included in the study. Results The results demonstrated that testosterone levels were lower in male alcoholics and higher in female alcoholics, as well as higher estrogen and cortisol levels in both genders. In addition, we found lower T3, T4, and thyroid-stimulating hormone (TSH) levels in alcoholics of both sexes. Furthermore, plasma TBARS, protein carbonyls, nitrite, and nitrate levels increased significantly with concomitant decrease in reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities in both male and female alcoholics. Furthermore, erythrocyte lysate nitrite and nitrate levels membrane total cholesterol, phospholipid and cholesterol/phospholipid (C/P) ratio with lower total membrane proteins in both genders of alcoholics. SDS-PAGE analysis of erythrocyte membrane proteins revealed increased density of band 3, protein 4.1, 4.2, 4.9 and glycophorins, whereas decreases in spectrin (α and β) were observed in both genders of alcoholics. Besides, alcoholics of both sexes had a lower ability to resist osmotic hemolysis. Plasma TBARS was negatively correlated with testosterone, TSH, T3 and T4 in male alcoholics, moreover, estradiol and cortisol were positively correlated in males and females respectively. Conclusion Female alcoholics may be more susceptible to osmotic hemolysis due to increased erythrocyte membrane lipid peroxidation with decreased antioxidant status, which results in an altered membrane C/P ratio and membrane protein composition.

Apoptotic and antioxidant activities of extracts of Spondias monbin stem bark in dimethylhydrazine (DMH)-induced colorectal carcinogenesis in Wistar rats

BackgroundColorectal cancer is the third most prevalent malignant neoplasm in the world and remains a leading cause of death, particularly in western nations. This study aimed to evaluate the apoptotic and antioxidant activities of Spondias mombin stem bark extracts in dimethylhydrazine (DMH) induced colon cancer in Wistar rats as well as to investigate the binding affinities of epicatechin, kaempferol and Lunamarin against p53 and caspase 3 proteins. MethodsA total of thirty-five (35) male Wistar rats were used for this experiment. They were grouped into five groups: Group 1 (normal control), Group 2 (DMH only- negative control), Group 3 (DMH + Xeloda - Standard Drug), Group 4 (DMH + 500 mg/kg bwt crude hydroethanol extracts), Group 5 (DMH + 500 mg bwt crude ethanol extracts. ResultsThe results showed high expression of proapoptotic genes which are Caspase-3 genes, B cell lymphoma 2 genes, and p53 genes and there was down regulation of antiapoptotic genes - Bcl like protein 4 genes. Also, the extracts of S. mombin stem bark attenuate the decreased antioxidant status (CAT, SOD and GSH) of DMN-induced colorectal cancer in rats and a significant decrease in the malondialdehyde levels. Molecular docking of the compounds (epicatechin, kaempferol and Lunamarin) against caspase 3 proteins possesses strong binding affinities with binding energies of -7.1, -7.0 and -7.5 kcal/mol respectively. However, kaempferol had similar binding energy(-7.0 kcal/mol) when docked against p53 gene. ConclusionTherefore, from the study, it was concluded that Spondias mombin stem bark has apoptotic and antioxidant properties.

Actinidia deliciosa Extract as a Promising Supplemental Agent for Hepatic and Renal Complication-Associated Type 2 Diabetes (In Vivo and In Silico-Based Studies).

Type 2 diabetes (T2D) is a chronic metabolic condition associated with obesity, oxidative stress-mediated inflammation, apoptosis, and impaired insulin signaling. The utilization of phytochemical therapy generated from plants has emerged as a promising approach for the treatment of diabetes and its complications. Kiwifruit is recognized for its substantial content of antioxidative phenolics. Therefore, this work aimed to examine the effect of Actinidia deliciosa (kiwi fruit) on hepatorenal damage in a high-fat diet (HFD) and streptozotocin (STZ)-induced T2D in rats using in vivo and in silico analyses. An increase in hepatic and renal lipid peroxidation was observed in diabetic rats accompanied by a decrease in antioxidant status. Furthermore, it is important to highlight that there were observable inflammatory and apoptotic responses in the hepatic and renal organs of rats with diabetes, along with a dysregulation of the phosphorylation levels of mammalian target of rapamycin (mTOR), protein kinase B (Akt), and phosphoinositide 3-kinase (PI3K) signaling proteins. However, the administration of kiwi extract to diabetic rats alleviated hepatorenal dysfunction, inflammatory processes, oxidative injury, and apoptotic events with activation of the insulin signaling pathway. Furthermore, molecular docking and dynamic simulation studies revealed quercetin, chlorogenic acid, and melezitose as components of kiwi extract that docked well with potential as effective natural products for activating the silent information regulator 1(SIRT-1) pathway. Furthermore, phenolic acids in kiwi extract, especially syringic acid, P-coumaric acid, caffeic acid, and ferulic acid, have the ability to inhibit the phosphatase and tensin homolog (PTEN) active site. In conclusion, it can be argued that kiwi extract may present a potentially beneficial adjunctive therapy approach for the treatment of diabetic hepatorenal complications.

Evaluation of the ameliorative potential of Nutritional Dietary supplementation of vitamin B12 following chronic tramadol hydrochloride exposure induced hyperlipidemia, atherogenic indices, and hepato-renal dysfunction by downregulating redox imbalance, NO/iNOS/NF-κB response, caspase-3- activation and DNA fragmentation in rat’s model

Vitamin B12 is an essential water-soluble vitamin, commonly found in a variety of foods. The present study investigated the effect of Vitamin B12 on tramadol-induced hepatorenal dysfunctionand DNA fragmentation in rats. Thirty-two (32) adult male Sprague–Dawley rats were randomized into four groups of eight (n=8) rats each. Group A served as control and was given 1 ml normal saline, group B received 50 mg /kg body weight (bwt) of tramadol (TRM), group C received 0.5 mg/kg bwt of vitamin B12 (VB12) and group D received 50 mg /kg bwt TRM and 0.5 mg/kg bwt of VB12 through gastric gavage daily for 8 weeks. The biomarkers of hepatorenal damage, antioxidant enzyme activities, myeloperoxidase (MPO), nitric oxide (NO), inducible nitric oxide synthase (iNOS), reactive oxygen and nitrogen (RONS) species and lipid peroxidation (LPO), lipid profile, tumour necrosis factor-alpha (TNF-α), nuclear factor-kappa B (NF-ĸB), interleukin-1 β (IL-1β) interleukin-6 (IL-6) and caspase-3 activity, cardiovascular risk indices, total ATPase, protein thiols, DNA fragmentation and liver and kidney histology were assessed.The increase in biomarkers of hepatorenal toxicity by TRM was alleviated by VB12. Also, the decrease in antioxidant status as well as the elevation in RONS and LPO were assuaged in rats cotreated with TRM and VB12. In addition, TRM-mediated increases in TNF-α, IL-1β, IL-6, NF-kB and caspase-3 activity were significantly diminished in the liver and kidney by VB12. Hepatorenal histopathological lesions were alleviated by VB12.Vitamin B12 therefore, assuaged TRM-induced oxidative stress, inflammation and caspase-3 activation in the liver and kidney.

Sodium benzoate exacerbates hepatic oxidative stress and inflammation in lipopolysaccharide-induced liver injury in rats

Background Liver damage is a global health concern associated with a high mortality rate. Sodium benzoate (SB) is a widely used preservative in the food industry with a wide range of applications. However, there’s a lack of scientific reports on its effect on lipopolysaccharide-induced hepatic dysfunction. Objective The present study investigated the influence of SB on lipopolysaccharide (LPS)-induced liver injury. Materials and methods Twenty-eight rats were randomly allocated into four groups: control (received distilled water), SB (received 600 mg/kg), LPS (received 0.25 mg/kg), and LPS + SB (received LPS, 0.25 mg/kg, and SB, 600 mg/kg). SB was administered orally for 14 days while LPS was administered intraperitoneally for 7 days. Results Administration of SB to rats with hepatocyte injury exacerbated liver damage with a significant increase in the activities of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP). We also observed that SB aggravated LPS-mediated hepatic oxidative stress occasioned by a marked decrease in antioxidant status with a concomitant increase in lipid peroxidation. Furthermore, LPS – mediated increase in inflammatory biomarkers as well as histological deterioration in the liver was exacerbated following the administration of SB to rats. Conclusion Taken together, the study provides experimental evidence that SB exacerbates hepatic oxidative stress and inflammation in LPS-mediated liver injury.

PROTECTIVE EFFECT OF ROSMARINUS OFFICINALIS EXTRACT ON THE NEPHROTOXICITY CAUSED BY NICKEL CHLORIDE IN WISTAR RATS

Nickel is a common environmental pollutant inducing nephrotoxicity. Oxidative stress has been proposed as a possible mechanism involved in this toxicity. The present study aimed to elucidate the potential protective effect of methanolic extract of Rosmarinus officinalis (RO) against nephrotoxicity induced by Nickel Chloride (NiCl2). The antioxidant activity and the metal chelating power of the plant extract were evaluated. An in vivo study on 28 rats divided into equal four groups including the first group as the control; the second received 100 mg/kg bw of RO extract; the third was exposed to 10 mg/kg bw of NiCl2, and the last was treated with the combination of the extract and NiCl2 by gavage for 28 days. Oxidative stress parameters, biochemical biomarkers, and histopathological examination of the kidney were determined. Analysis of the results showed that the plant has significant antioxidant and metal-chelating power. In addition, exposure of rats to NiCl2 caused a disturbance of renal function (urea, creatinine, and uric acid). This exposure also induced a renal oxidative stress, which results in increased MDA level and GST activity a decrease in antioxidant status (CAT, GPx, and SOD activity), and alteration in tissue architecture of kidney was observed. Co-administration of RO (extract and NiCl2) restored most of the parameters cited above to values close to normal. Therefore, the present study revealed the ability of RO to bind to NiCl2 and protect kidney tissue from NiCl2-induced oxidative damage.

Oxidative Stress in Primary Bone Tumors: A Comparative Analysis.

BackgroundBone tumors account for 1% of all cancers and have considerable morbidity and mortality. There is a proposed theory of increased oxidative stress characterized by an increased level of reactive oxygen species (ROS) that disrupts the intracellular reduction-oxidation (redox) balance which has been implicated in various diseases including cancer. The aim of the present study was to measure the levels of oxidant stress and antioxidant mechanism in bone tumors (benign as well as malignant). MethodsThe study cohort consisted of 42 subjects: 14 malignant bone tumors, 14 benign bone tumors, and 14 healthy controls. Serum Malondialdehyde (MDA) levels were determined to assess oxidative stress while antioxidant status was evaluated using superoxide dismutase (SOD).ResultsPatients with malignant bone tumors showed a significant increase in plasma MDA levels (p<0.05) while SOD levels were significantly decreased (p<0.05). No significant difference in oxidative damage was noted between both the sarcomas (p>0.05).ConclusionsIn conclusion, an increase in oxidative stress and a decrease in antioxidant status are observed in bone tumors. Further studies on the manipulation of redox balance in patients with bone tumors can act as a useful approach in early diagnosis or designing management strategies for bone tumors.

Role of Glutathione-S-Transferase M1 (GSTM1) and T1 (GSTT1) Genes on Aluminum Concentration and Oxidative Markers among Autistic Children

Autism Spectrum Disorder (ASD) is considered a multifaceted neurodevelopmental disorder. The last two decades showed an increase in its prevalence until reached about 1 in 54 children. Autistic symptoms may be exacerbated when the interaction of the genetic and the environmental risk factors occur, suggesting that gene-environment interaction could be a mechanism underlying the etiology of ASD. Aluminum is a known neurotoxic metal that has known health effects in humans. Glutathione-S-transferase (GST) genes and their enzymes play a major role in the detoxification of many toxic metals.Data were collected from 76 children aged 2-8 years diagnosed with ASD and 30 sex and age matched healthy children. The aim of this study was to investigate the association of polymorphisms in the two GST genes (GSTM1 and GSTT1) with mean aluminum concentrations (as, gene-environment interaction) and oxidative status markers (GST enzyme, malondialdehyde and nitric oxide) among the studied groups. The study started at December 2019 and last for one year at the clinics of National Research Centre, Egypt.The results of this study showed that the null GSTM1 and GSTT1 genotype is the most common type in ASD and that genotype may predispose ASD children to decreased antioxidant status (GST enzyme activity) which in term lead to mal detoxification of aluminum. There is marked increase in aluminum concentrations in hair of ASD children and oxidative markers (increase in MDA and NO) leading to oxidative damage that may play an important role in children autistic status. The study recommends adding antioxidant supplements to daily diet of ASD children to improve their antioxidant status and in term improving management of patients with autism spectrum disorders. Further studies are needed to describe other GST gene polymorphisms.

Protocatechuic acid protects against hepatorenal toxicities in rats exposed to Furan

Furan formed in processed food is hepatotoxic and likely carcinogenic in humans. We investigated protocatechuic acid (PCA) protective role in rats’ hepatorenal function treated with furan. Rats were grouped and treated as follows: Control, PCA (50 mg/kg), furan alone (8 mg/kg), furan + PCA1 (25 + 8 mg/kg), and furan + PCA2 (50 + 8 mg/kg). Upon sacrifice, evaluation of hepatorenal function, oxidative stress status, reactive oxygen and nitrogen species (RONS), lipid peroxidation (LPO), myeloperoxidase (MPO) activity, among nitric oxide (NO) levels were performed. Cytokine levels (IL-10, IL-1ß, TNF-alpha), Caspase 3 and 9 activities, and histopathological examination were also assessed. We found that the final body and relative liver weights changed significantly (p < 0.05) in treated groups. Hepatic transaminases, urea, and creatinine increased (p < 0.05) in furan only treated group, and reduced in PCA co-treated groups. The furan-induced decrease in antioxidant status increased RONS, and LPO levels were alleviated (p < 0.05) by PCA co-treatment. Furthermore, furan-mediated increase in NO, IL-1ß, TNF-alpha levels, MPO, Cas-3, and 9 activities and suppressed IL-10 levels was reversed accordingly in rats’ kidney and liver co-treated with PCA. The extent of furan-mediated hepatorenal lesions was lessened in PCA co-treated rats. Our findings suggest that PCA protects against oxido-inflammatory pathways, enhanced caspases 3 and 9 activations induced by furan in rat hepatorenal system.

Monosodium glutamate induces memory and hepatic dysfunctions in mice: ameliorative role of Jobelyn® through the augmentation of cellular antioxidant defense machineries.

This study investigated the effect of high doses of monosodium glutamate (MSG), a known food additive on hepatic, memory and locomotor functions in mice, and the ameliorative potentials of Jobelyn® (JB), a unique dietary supplement. Twenty four male Swissmice divided into 4 groups (n = 6) were given MSG (2, 4 and 8g/kg) or normal saline (10mL/kg) orally for 14days. In the intervention study, another set of 30 male Swissmice distributed into 5 groups (n = 6) received normal saline,MSG (8g/kg) alone or in combination with JB (5, 10 and 20mg/kg) orally, for 14days. Memory and locomotor functions as well as brain oxido-nitrergic stress biomarkers were then assessed in both studies. The hepatic oxido-nitrergic stress biomarkers, liver enzymes functions and histomorphology of the liver were also assessed. MSG (2, 4 and 8g/kg) produced memory dysfunction, hyperlocomotion, increased malondialdehyde and nitrite levels accompanied by decreased antioxidant status in the brain and hepatic tissues. MSG-treated mice had increased hepatic enzyme activities (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase) and distorted cyto-architectural integrity of the liver. These findings further suggest that MSG compromised hepatic functioning, which might also contribute to its neurotoxicity. However, JB (5, 10 and 20mg/kg, p.o) attenuated the memory deficit, hyperlocomotion, increased oxido-nitrergic stress responses in the brain and hepatic tissues induced by MSG (8g/kg, p.o). JB also normalized hepatic enzymes activities and histomorphological changes in MSG-treated mice. Taken together, JB mitigated MSG-induced toxicity through mechanisms relating to enhancement of cellular antioxidant-machineries and normalization of hepatic enzymatic functions.

Study on Glycemic Statusand Oxidative Stress Level in Patients of Type 2 Diabetes Mellitus With and Without Retinopathy: A Teaching Hospital Based Study

Background: Diabetes is a chronic disease and sustained hyperglycemia attacks both micro vessels and macro vessels throughout the body. It is the leading cause of retinopathy, nephropathy, end-stage renal disease, non traumatic lower extremity amputations.Subjects and Methods:Twenty five (25) Patients with newly diagnosed type 2 diabetes mellitus without any signs of retinopathy were identified from outpatient services of department of Medicine and Twenty five (25) Patients with newly diagnosed type 2 diabetes mellitus with retinopathy were identified from outpatient services of department of Ophthalmology along with 25 healthy subjects were taken as controls. Diabetic retinopathy was diagnosed after doing detailed dilated fundoscopic examination as per the standard criteria.Results:The levels of FBS, HbA1c, total cholesterol, triglycerides and MDA were significantly higher in the diabetics without retinopathy, while the HDL and Vitamin C levels were lower as compared to those of the control group. The levels of FBS HbA1c, cholesterol, triglycerides and MDA were significantly higher in the diabetics with retinopathy, while the HDL and Vitamin C levels were lower as compared to those in the diabetes without retinopathy.Conclusion: The increased oxidative stress and a decreased antioxidant status can predict the micro-vascular complications in diabetes mellitus. The raised MDA levels indicate the oxidative stress and the decreased Vitamin C levels indicate the reduced antioxidant status in diabetic retinopathy.

Effect of cocoa powder on hypertension and antioxidant status in uninephrectomized hypertensive rats.

Background and Aim:High salt diet and uninephrectomy are associated with high blood pressure with attendant cardiovascular disease conditions such as hypertension, renal damage, myocardial infarction, and stroke. The aim of this study was to investigate the beneficial effects of consumption of cocoa and cocoa-containing products in the management of high blood pressure in uninephrectomized hypertensive rats.Materials and Methods:The effect of cocoa powder on blood pressure, markers of inflammation, oxidative stress, and histopathology were investigated in uninephrectomized animals fed with cocoa feed alone or in combination with a high salt diet. Male rats were randomly divided into five groups: Group A was the control group and fed with normal feed alone, Group B was fed with cocoa feed alone, Group C was fed with high salt diet (8% salt), GroupD was fed with cocoa-feed compounded with 8% salt for 4weeks after uninephrectomy, and GroupE was uninephrectomized rats on a normal diet. The left kidneys of animals in GroupsC, D, and E were removed by surgery. After 4weeks of treatment, the systolic, diastolic, and mean arterial blood pressure was measured. The serum markers of renal damage and oxidative stress were determined. Histological examination was also performed on renal and cardiac tissues.Results:Results showed significant increases in biomarkers of oxidative stress, inflammation, and renal damage with a concomitant decrease in antioxidant status in hypertensive uninephrectomized rats. Cocoa feed, however, significantly improved blood pressure and nitric oxide bioavailability, antioxidant status and reduced markers of inflammation and oxidative stress.Conclusion:These findings show that cocoa powder could be used to maintain blood pressure levels in hypertensive rats through its antioxidant capacity.

Edaravone and benidipine protect myocardial damage by regulating mitochondrial stress, apoptosis signalling and cardiac biomarkers against doxorubicin-induced cardiotoxicity

ABSTRACTBackground: Doxorubicin (DOX) is a potential chemotherapeutic agent but its use is restricted due to cardiotoxicity. Edaravone is a potent-free radical scavenging agent used in cerebral ischaemia. Benidipine is a triple calcium channel blocker.Objective: We investigated the potential cardioprotective effects of edaravone and benidipine alone and their combination against DOX-induced cardiotoxicity. Cardiotoxicity was induced by administering six equal injections of DOX (2.5 mg/kg) on alternative days for 2 weeks.Result: DOX-treated group showed significant increase level of lipid peroxide and decrease in antioxidant status along with mitochondrial enzymatic activity. Cardiotoxity effect of DOX illustrated by significantly increased the cardiac biomarkers such as Cardiac troponin-I, Brain natriuretic peptide, Creatine kinase-MB in serum. Significant increased activation of TNF-α, Caspase-3 activity and myocardial infarct size in DOX-treated group. Histopathological evaluation also confirmed the DOX-induced cardiotoxicity. Pretreated with edaravone and benidipine was significantly attenuated level of thiobarbituric acid reactive substance, endogenous enzymes, mitochondrial enzyme activities and cardiac biomarkers. Furthermore, pretreated group showed decreased activation of TNF-α, Caspase-3 activity along with reduction in the myocardial infarct size. Histopathological evaluation also strengthened the above results.Conclusion: Taken together these results suggest that the pretreated with edaravone and benidipine have potential protective effect against DOX-induced cardiotoxicity.

Histopathological and ultrastructural studies on the protective effect of daidazein and vitamin C against gamma irradiation induced kidney alterations in albino rats

Introduction: Radiotherapy is an important therapeutic manner of a wide range of tumors. Its side effects on normal cells limit the efficiency of therapy.Aim of the work: To evaluate the protective role of daidzein and/or vitamin C against biochemical, histopathological and ultrastructural changes in male albino rats exposed to gamma radiation (γ-radiation).Materials and Methods: The whole-body exposed to 8 GY γ-radiation. Daidzein was given to rats at a concentration of 63 mg/kg b.wt./day for 7 days before irradiation and 7 days during exposure. Whereas vitamin C was ingested at a concentration of 5 mg/kg b.wt. /day for 7 days before irradiation and 7 days during exposure. Animals were sacrificed on the 1st day post the irradiation dose. Blood samples were collected for biochemical determination of uric acid, urea, and creatinine. Lipid peroxides (TBARS) concentration and the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were also measured. Samples from the kidney were processed for light and electron microscopy.Results: Irradiation induced significant elevation in uric acid, urea, creatinine and TBARS. These changes were accompanied by significant decrease in antioxidant status (SOD, CAT, and GPx). Also, the histological and ultrastructural investigation displayed remarkable changes in kidney tissue. Daidzein and /or vitamin C reduced the kidney damage induced by irradiation; this was showed by declined levels of creatinine, urea and uric acid, in addition to increased CAT, GPx, and SOD activities. The histopathological structure and ultrastructural alternations were also improved. The radioprotection index for the combination of daidzein and vitamin C was found to be more than daidzein or vitamin C separately. Conclusion: Daidzein and vitamin C might modulate radiation damages to kidney by boosting the antioxidant capacity and attenuating oxidative injury.

Manganese suppresses oxidative stress, inflammation and caspase-3 activation in rats exposed to chlorpyrifos.

The present study investigated the individual and combined impact of organophosphorus pesticide chlorpyrifos (CPF) and manganese (Mn), a naturally occurring trace metal, on hepatorenal function in adult rats. The four experimental groups namely control, CPF alone (5 mg/kg), Mn alone (10 mg/kg) and the co-exposure group consisted of eight rats which were orally gavage for 14 consecutive days. Following sacrifice, the biomarkers of hepatorenal damage, antioxidant enzyme activities, myeloperoxidase (MPO) activity as well as levels of nitric oxide, reactive oxygen and nitrogen (RONS) species and lipid peroxidation (LPO) were analysed spectrophotometrically. Further, the concentration of tumour necrosis factor alpha (TNF-α), interleukin-1 β (IL-1β) and caspase-3 activity were assessed using ELISA. Results showed that the CPF-induced increase in biomarkers of hepatorenal toxicity were significantly (p < 0.05) alleviated in rats co-expose to CPF and Mn. Moreover, the decrease in antioxidant status as well as the elevation in RONS and LPO were significantly assuaged in rats co-treated with CPF and Mn. In addition, CPF mediated increase in TNF-α, IL-1β and caspase-3 activity were significantly diminished in the liver and kidney of rats co-exposed to CPF and Mn. Light microscopic examination evidenced that the severity of histopathological lesions induced by CPF were alleviated in rats co-exposed to CPF and Mn. In conclusion, the results highlight that co-exposure to CPF and Mn in rats assuaged CPF-induced oxidative stress, inflammation and caspase-3 activation in the liver and kidney of the rats.

Biochemical alterations in diclofenac-treated rats: Effect of selenium on oxidative stress, inflammation, and hematological changes

We investigated the effect of selenium (Sel), a trace element in diclofenac sodium (DCF), nonsteroidal anti-inflammatory drugs-induced hepatic and renal toxicities in adult rats. Five experimental groups namely control, DCF (10 mg/kg), Sel (0.125 mg/kg), DCF + Sel (0.125 mg/kg), and DCF + Sel (0.25 mg/kg) consisting of 10 rats each were orally treated for 7 consecutive days. Following killing, biomarkers of hepatic and renal toxicities, antioxidant enzyme levels, myeloperoxidase activity, nitric oxide levels, reactive oxygen and nitrogen species (RONS), and lipid peroxidation (LPO) were analyzed spectrophotometrically. Further, the concentration of tumor necrosis factor alpha (TNF-α) was assessed using enzyme-linked immunosorbent assay, and hematological indices: white blood cells (WBC), lymphocytes, and neutrophils and eosinophil counts. Results indicated that DCF-induced increases in biomarkers of hepatic and renal toxicity were significantly ( p &lt; 0.05) lessened in serum of rats co-exposed to DCF and Sel in a dose-dependent manner. DCF mediated decrease in antioxidant status, and increases in RONS, LPO, and TNF-α levels were reduced ( p &lt; 0.05) in the liver and kidney of rats co-exposed to DCF and Sel. Additionally, Sel reduced hematological abnormalities associated with DCF treatment. Light microscopic examination showed that the severity of histopathological lesions induced by DCF was lessened in rats co-exposed to DCF and Sel. Taken together, Sel supplementation mitigated DCF-induced oxidative stress, inflammation, and hematological abnormalities in the liver and kidney of treated rats.

Long term Westernized diet leads to region-specific changes in brain signaling mechanisms

Western diets, high in fat and energy, are associated with cognitive deficits in humans and animal models, but the underlying mechanisms are not fully elucidated. This includes whether diet-induced dyslipidemia per se negatively impacts brain signaling. Here we investigate the effects of dyslipidemia induced by two high fat diets with or without high sucrose on hippocampal and frontal cortical oxidative stress, brain-derived neurotrophic factor (BDNF) and down-stream markers of synaptic plasticity, as well as alterations in monoaminergic neurotransmitter levels. A high fat diet was associated with decreased antioxidant status (vitamin C), increased serotonin in the frontal cortex, and increased ratio of phosphorylated Ca2+/calmodulin-dependent protein kinase II in the hippocampus, while a high fat and sucrose diet decreased levels of vitamin C in the frontal cortex and BDNF in the hippocampus. Markers of dyslipidemia correlated significantly with cerebral vitamin C levels, monoaminergic neurotransmitters and metabolites in the frontal cortex, but not in the hippocampus. Thus, a high fat diet caused regional alterations in antioxidant levels, neurochemistry and molecular markers in the non-obese dyslipidemic guinea pig.

Ram semen deterioration by short-term exposure to high altitude is prevented by improvement of antioxidant status

Ovine reproduction efficiency in herds at high altitude (ha) is lower than that at low altitude (la). In ewes, ha effects are due to hypoxia and oxidative stress. Our aim was to establish the effect of antioxidant vitamin supplementation on semen traits and antioxidant status of rams exposed to short or long time ha. A total of 32 rams native to la (~500 m) were used, 16 were kept at la and the other 16 were brought to ha (~3600 m), where they were placed in the same flock as the ha native rams (n=16). Half of the animals in each group were supplemented daily with vitamins C 600 mg and E 450 IU per os, during the entire experimental period, starting the 4th day after animal’s arrival at ha (day 0). At days 0, 30 and 60 of treatment, blood and semen samples were collected for evaluation of antioxidant status and semen standard characteristics. Data were compared within each experimental time by analysis of variance using a general linear model. Elevated concentrations of oxidative stress biomarkers were present in blood from animals maintained at ha. Ejaculates from ha exposed rams showed decreased sperm concentration, progressive motility and viability, in addition to decreased antioxidant status in seminal fluid. A total of 30 days of oral supplementation with vitamins C and E prevented some ha negative effects on semen characteristics, mainly in recently ha exposed rams. It is concluded that exposure of rams to ha negatively affects semen quality, where oxidative stress plays a predominant role. These effects are mainly prevented by oral supplementation of vitamins C and E, which constitutes a simple and cheap alternative to improve semen quality of rams when they are moved to ha.

ANTIOXIDANT STATUS OF PATIENTS WITH ATHEROTHROMBOTIC VARIANT OF ISCHEMIC STROKE

Aim. To study the dependence of antioxidant status (AOS) on the age, sex, localization and size of the damage focus in patients during the most acute period of the development of atherothrombotic variant of ischemic stroke. Materials and methods. Seventy four patients (main group) in the most acute period of atherothrombotic variant of ischemic stroke were examined. The group of comparison, comparable by age and sex, included 15 healthy persons. The total blood serum antioxidant status was investigated using an assay kit of “Vector-Best” Company B-7501 (“Vector-Best”, Russia). Results. AOS value in the comparison group was 1,69 ± 0,17 mmol/l (median 1,72; interquartile range 1,53-1,83 mmol/l) that corresponded to the standard interval, indicated in the assay kit guidelines (1,3-1,8 mmol/l). OAS did not differ in men and women (criterion U = 26,0; p = 0,816). In patients of the main group, AOS was reduced ( p = 0,000034); AOS value was 1,14 ± 0,4 mmol/l (median 1,12 mmol/l, interquartile range 0,81-1,45 mmol/l). Age, sex and localization of stroke focus did not reliably influence the degree of AOS fall. Moderate reverse correlation between the focal sizes and decreased AOS value was established. Spearman’s rank correlation coefficient was -0,79 ( p &lt; 0,001). Conclusions. Decrease in AOS during the most acute period of developing atherothrombotic stroke does not depend on sex, age, ischemic focus localization, but it depends on sizes of the focus, subjected to ischemization.