Neurological Alterations and Testicular Damages in Aging Induced by D-Galactose and Neuro and Testicular Protective Effects of Combinations of Chitosan Nanoparticles, Resveratrol and Quercetin in Male Mice

Aging is a neurological disease that is afforded by incidence of oxidative stress. Chitosan has received global interests due to its wide medical uses. Quercetin (Q) is a bioflavonoid and widely distributed in vegetables and fruits. Resveratrol is considered as a potent antioxidant and is a component of a wide range of foods. The using of either chitosan nanopartciles (CH-NPs), querectin (Q), and resveratrol (RV) to reduce the oxidative stress and biochemical alterations on brain and testicular tissues induced by D-galactose (DG) (100 mg/Kg) were the aim of the present study. This study investigated the probable protective effects of CH-NPs in two doses (140,280 mg/Kg), Q (20 mg/Kg) and RV (20 mg/Kg), against DG induced aging and neurological alterations. Brain antioxidant capacity as malonaldehyde (MDA), catalase (CAT), and glutathione reductase (GRx), as well as histopathological damages of the brain and testicular tissues were measured. The DG treated group had significantly elevated the oxidative stress markers by 96% and 91.4% in brain and testicular tissues respectively and lower significantly the antioxidant enzyme activities of both brain and testicular tissues than those of the control group by 86.95%, 69.27%, 83.07%, and 69.43%. Groups of DG that treated with a combination of CH-NPs in two doses, Q and RV, the levels of oxidative stress marker declined significantly by 68.70%, 76.64% in brain tissues and by 74.07% and 76.61% in testicular tissues, and the enzymatic antioxidants increased significantly by 75.55%, 79.24%, 62.32%, and 61.97% as compared to the DG group. The present results indicate that CH-NPs, Q, and RV have protective effects against DG-induced brain and testis tissue damage at the biochemical and histopathological levels. Mechanisms of this protective effect of used compounds against neurological and testicular toxicity may be due to the enhanced brain and testis antioxidant capacities.

Download Full-text

Chitosan/Selenium Nanoparticles Attenuate Diclofenac Sodium-Induced Testicular Toxicity in Male Rats

Crystals ◽

10.3390/cryst11121477 ◽

2021 ◽

Vol 11 (12) ◽

pp. 1477

Author(s):

Samy M. El-Megharbel ◽

Fawziah A. Al-Salmi ◽

Sarah Al-Harthi ◽

Khadeejah Alsolami ◽

Reham Z. Hamza

Keyword(s):

Oxidative Stress ◽

Diclofenac Sodium ◽

Chitosan Nanoparticles ◽

Reproductive Toxicity ◽

Male Reproduction ◽

Male Rats ◽

Antioxidant Enzyme Activities ◽

Testicular Function ◽

Wide Range ◽

The Impact

The detrimental effect of diclofenac sodium (Diclo-Na) on male reproductive organs is reported upon in this paper. Chitosan is a polysaccharide composed of various amounts of glucosamine. Chitosan nanoparticles (CH-NPs) have attracted much attention owing to their biomedical activity. Selenium (Se) has a vital role in nutrition, plays an important role in enhancing male reproduction, and has a wide range of free radical scavenging activities. However, the study of the impact of chitosan nanoparticles in combination with Se (IV) (CH-NPs/Se) on male reproductive toxicity associated with Diclo-Na administration is lacking in recent literature. The current study assessed the ameliorative effects of complexes of CH-NPs/Se (IV) on Diclo-Na and the ways in which they alter reproductive toxicity in male rats. Male rats were treated for 30 days successively, either with Diclo-Na (10 mg/kg) or co-treated with a CH-NPs/Se complex (280 mg/kg). Sperm characteristics, marker enzymes of testicular function, LH, FSH, and testosterone were evaluated in addition to oxidative stress markers and histological alterations. CH-NPs/Se significantly alleviated Diclo-Na-induced decline in sperm count and motility, testicular function enzymes, and levels of LH and testosterone in serum. Additionally, CH-NPs/Se co-administration at 280 mg/Kg, inhibited the Diclo-Na-induced decline of antioxidant enzyme activities and elevated oxidative stress indices and reactive free radicals in testicular homogenates of male rats. CH-NPs/Se (280 mg/kg) alone improved Diclo-Na and ameliorated histological damages in exposed rats. In conclusion, chitosan improved testicular function in Diclo-Na-treated rats by enhancing the testosterone hormone levels, ameliorating testicular tissue, and inhibiting markers of oxidative stress in male rats.

Download Full-text

Celastrol pretreatment as a therapeutic option against cisplatin-induced nephrotoxicity

Toxicology Research ◽

10.1039/c9tx00141g ◽

2019 ◽

Vol 8 (5) ◽

pp. 723-730 ◽

Cited By ~ 1

Author(s):

Tugce Boran ◽

Aysenur Gunaydin ◽

Ayse Tarbin Jannuzzi ◽

Eren Ozcagli ◽

Buket Alpertunga

Keyword(s):

Oxidative Stress ◽

Therapeutic Potential ◽

Antioxidant Activities ◽

Rat Kidney ◽

Therapeutic Option ◽

Control Group ◽

Epithelial Cell Line ◽

Protective Effects ◽

Wide Range ◽

Significant Difference

Abstract Celastrol is a natural bioactive compound extracted from the medicinal plant Tripterygium wilfordii Hook F. It exhibits immunosuppressive, anti-inflammatory, and antioxidant activities. Cisplatin is a commonly used chemotherapeutic drug in the treatment of a wide range of tumors. Although very effective therapeutically, it can cause nephrotoxicity leading to dose reduction or discontinuation of treatment. This study aims to clarify the therapeutic potential of celastrol in cisplatin-induced nephrotoxicity. The possible protective effects of celastrol pretreatment against cisplatin-induced oxidative stress and genotoxicity were investigated. A rat kidney epithelial cell line NRK-52E was pretreated with the desired concentrations of celastrol (200 nM, 100 nM, and 50 nM) for 24 h. The cells were treated with 50 μM cisplatin for a further 24 h to see whether cisplatin caused the same or less toxicity compared to the vehicle control group. Alkaline comet assay was performed for genotoxicity assessment. Genotoxicity evaluation revealed that celastrol caused a statistically significant reduction in DNA damage. Oxidative stress parameters were evaluated by measuring the glutathione (GSH) and protein carbonyl (PC) levels and also by measuring the enzyme activities of glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT) and superoxide dismutase (SOD) enzymes. Celastrol pretreatment increased the GSH content of the cells and ameliorated the protein carbonylation level. Likewise, celastrol pretreatment improved the GR and CAT activities. However, no significant difference was observed in GPx and SOD activities. In the light of these findings, celastrol treatment could be a therapeutic option to reduce cisplatin-induced nephrotoxicity. Further studies are needed for the clarification of its therapeutic potential.

Download Full-text

Oxidative Stress Status in Patients with Choledocholithiasis: Before and After Endoscopic Sphincterotomy and Biliary Clearance

Revista de Chimie ◽

10.37358/rc.18.8.6493 ◽

2018 ◽

Vol 69 (8) ◽

pp. 2172-2176

Author(s):

Catalin Victor Sfarti ◽

Alin Ciobica ◽

Carol Stanciu ◽

Gheorghe G. Balan ◽

Irina Garleanu ◽

...

Keyword(s):

Oxidative Stress ◽

Endoscopic Sphincterotomy ◽

Specific Activity ◽

Oxidative Stress Marker ◽

Control Group ◽

Oxidative Stress Parameter ◽

Extrahepatic Cholestasis ◽

Biliary Clearance ◽

Oxidative Stress Status ◽

Before And After

Choledocholithiasis may cause biliary obstruction which leads to hepatocellular injury. Oxidative stress has been proposed as a possible mechanism involved in this disorder. This study evaluates the oxidative stress burden in patients with choledocholithiasis and secondary cholestasis, before and after endoscopic sphincterotomy. Experimental part: Patients diagnosed with choledocholithiasis and secondary extrahepatic cholestasis were included in the study between January 1st 2016 and October 31st 2016. In all patients oxidative stress markers were collected within 2 hours before and 48 hours after therapeutic ERCP. Selected markers were superoxide dismutase (SOD), glutathione peroxidase (GPX) and malondialdehyde (MDA). The results were compared to those from a group of 40 healthy subjects. Significantly lower concentrations of SOD (p = 0.03) and GPX (p [ 0.0001) activities, associated with an increased level of MDA level (p [ 0.0001) were shown in patients before biliary clearance compared with the healthy control group. After ERCP the only oxidative stress parameter which showed improvement was the SOD specific activity (p = 0.037). This study shows that extrahepatic cholestasis secondary to choledocholithiasis is associated with increased oxidative stress status. After biliary clearance one oxidative stress marker was significantly improved (SOD), suggesting a possible antioxidant effect of such procedure.

Download Full-text

Protective Effects of Taurine Chloramine on Experimentally Induced Colitis: NFκB, STAT3, and Nrf2 as Potential Targets

Antioxidants ◽

10.3390/antiox10030479 ◽

2021 ◽

Vol 10 (3) ◽

pp. 479

Author(s):

Seong Hoon Kim ◽

Hye-Won Yum ◽

Seung Hyeon Kim ◽

Wonki Kim ◽

Su-Jung Kim ◽

...

Keyword(s):

Oxidative Stress ◽

Protective Effect ◽

Parent Compound ◽

Oxidative Stress Marker ◽

Heme Oxygenase 1 ◽

Trinitrobenzene Sulfonic Acid ◽

Protective Effects ◽

Taurine Chloramine ◽

Proinflammatory Mediators ◽

Experimentally Induced

Taurine chloramine (TauCl) is an endogenous anti-inflammatory substance which is derived from taurine, a semi-essential sulfur-containing β-amino acid found in some foods including meat, fish, eggs and milk. In general, TauCl as well as its parent compound taurine downregulates production of tissue-damaging proinflammatory mediators, such as chemokines and cytokines in many different types of cells. In the present study, we investigated the protective effects of TauCl on experimentally induced colon inflammation. Oral administration of TauCl protected against mouse colitis caused by 2,4,6-trinitrobenzene sulfonic acid (TNBS). TauCl administration attenuated apoptosis in the colonic mucosa of TNBS-treated mice. This was accompanied by reduced expression of an oxidative stress marker, 4-hydroxy-2-nonenal and proinflammatory molecules including tumor necrosis factor-α, interleukin-6 and cyclooxygenase-2 in mouse colon. TauCl also inhibited activation of NFκB and STAT3, two key transcription factors mediating proinflammatory signaling. Notably, the protective effect of TauCl on oxidative stress and inflammation in the colon of TNBS-treated mice was associated with elevated activation of Nrf2 and upregulation of its target genes encoding heme oxygenase-1, NAD(P)H:quinone oxidoreductase, glutamate cysteine ligase catalytic subunit, and glutathione S-transferase. Taken together, these results suggest that TauCl exerts the protective effect against colitis through upregulation of Nrf2-dependent cytoprotective gene expression while blocking the proinflammatory signaling mediated by NFκB and STAT3.

Download Full-text

Antioxidant activity of Lactobacillus plantarum NJAU-01 in an animal model of aging

BMC Microbiology ◽

10.1186/s12866-021-02248-5 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Qingfeng Ge ◽

Bo Yang ◽

Rui Liu ◽

Donglei Jiang ◽

Hai Yu ◽

...

Keyword(s):

Oxidative Stress ◽

Antioxidant Capacity ◽

Lactobacillus Plantarum ◽

Meat Product ◽

The Other ◽

Oxidative Stress Marker ◽

Control Group ◽

Intragastric Administration ◽

Aging Effects ◽

Sterile Saline

Abstract Background Excessive reactive oxygen species (ROS) can cause serious damage to the human body and may cause various chronic diseases. Studies have found that lactic acid bacteria (LAB) have antioxidant and anti-aging effects, and are important resources for the development of microbial antioxidants. This paper was to explore the potential role of an antioxidant strain, Lactobacillus plantarum NJAU-01 screened from traditional dry-cured meat product Jinhua Ham in regulating D-galactose-induced subacute senescence of mice. A total of 48 specific pathogen free Kun Ming mice (SPF KM mice) were randomly allocated into 6 groups: control group with sterile saline injection, aging group with subcutaneously injection of D-galactose, treatments groups with injection of D-galactose and intragastric administration of 107, 108, and 109 CFU/mL L. plantarum NJAU-01, and positive control group with injection of D-galactose and intragastric administration of 1 mg/mL Vitamin C. Results The results showed that the treatment group of L. plantarum NJAU-01 at 109 CFU/mL showed higher total antioxidant capacity (T-AOC) and the antioxidant enzymatic activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) than those of the other groups in serum, heart and liver. In contrast, the content of the oxidative stress marker malondialdehyde (MDA) showed lower levels than the other groups (P < 0.05). The antioxidant capacity was improved with the supplement of the increasing concentration of L. plantarum NJAU-01. Conclusions Thus, this study demonstrates that L. plantarum NJAU-01 can alleviate oxidative stress by increasing the activities of enzymes involved in oxidation resistance and decreasing level of lipid oxidation in mice.

Download Full-text

Glycine and L-Arginine supplementation ameliorates gastro-duodenal toxicity in a rat model of NSAID (Diclofenac)-gastroenteropathy via inhibition of oxidative stress

Journal of Basic and Clinical Physiology and Pharmacology ◽

10.1515/jbcpp-2020-0307 ◽

2021 ◽

Vol 0 (0) ◽

Author(s):

Akinleye Stephen Akinrinde ◽

Halimot Olawalarami Hameed

Keyword(s):

Oxidative Stress ◽

Total Protein ◽

Therapeutic Index ◽

Control Treatment ◽

Control Group ◽

Protective Effects ◽

Serum Total Protein ◽

Significant Amelioration ◽

Group A ◽

Group B

Abstract Objectives This study examined the possible protective roles of exogenous glycine (Gly) and L-Arginine (l-Arg) against Diclofenac (DIC)-induced gastro-duodenal damage in rats. Methods Rats were divided into Group A (control), Group B (DIC group) and Groups C–F which were pre-treated for five days with Gly1 (250 mg/kg), Gly2 (500 mg/kg), l-Arg1 (200 mg/kg) and l-Arg2 (400 mg/kg), respectively, before co-treatment with DIC for another three days. Hematological, biochemical and histopathological analyses were then carried out. Results DIC produced significant (p<0.05) reduction in PCV (13.82%), Hb (46.58%), RBC (30.53%), serum total protein (32.72%), albumin (28.44%) and globulin (38.01%) along with significant (p<0.05) elevation of serum MPO activity (83.30%), when compared with control. In addition, DIC increased gastric H2O2 and MDA levels by 33.93 and 48.59%, respectively, while the duodenal levels of the same parameters increased by 19.43 and 85.56%, respectively. Moreover, SOD, GPx and GST activities in the DIC group were significantly (p<0.05) reduced in the stomach (21.12, 24.35 and 51.28%, respectively) and duodenum (30.59, 16.35 and 37.90%, respectively), compared to control. Treatment with Gly and l-Arg resulted in significant amelioration of the DIC-induced alterations although l-Arg produced better amelioration of RBC (29.78%), total protein (10.12%), albumin (9.93%) and MPO (65.01%), compared to the DIC group. The protective effects of both amino acids against oxidative stress parameters and histological lesions were largely similar. Conclusions The data from this study suggest that Gly or l-Arg prevented DIC-induced gastro-duodenal toxicity and might, therefore be useful in improving the therapeutic index of DIC.

Download Full-text

Attenuation of erythrocyte membrane oxidative stress bySesbania grandiflorain streptozotocin-induced diabetic rats

Biochemistry and Cell Biology ◽

10.1139/bcb-2015-0039 ◽

2015 ◽

Vol 93 (4) ◽

pp. 385-395 ◽

Cited By ~ 7

Author(s):

Chandrabose Sureka ◽

Thiyagarajan Ramesh ◽

Vavamohaideen Hazeena Begum

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Blood Glucose ◽

Erythrocyte Membrane ◽

Osmotic Fragility ◽

Diabetic Rats ◽

Glycosylated Haemoglobin ◽

Albino Rats ◽

Enzymatic Antioxidants ◽

Protective Effects

The aim of the present study was to investigate the protective effects of Sesbania grandiflora flower (SGF) extract on erythrocyte membrane in Streptozotocin (STZ)-induced diabetic rats. Adult male albino rats of Wistar strain, weighing 190–220 g, were made diabetic by an intraperitonial administration of STZ (45 mg/kg). Normal and diabetic rats were treated with SGF, and diabetic rats were also treated with glibenclamide as drug control, for 45 days. In this study plasma insulin and haemoglobin levels were decreased and blood glucose, glycosylated haemoglobin, protein oxidation, lipid peroxidation markers, and osmotic fragility levels were increased in diabetic rats. Moreover, erythrocytes antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxide, glutathione reductase, glutathione-S-transferase, and glucose-6-phosphate dehydrogenase activities and non-enzymatic antioxidants such as vitamin C, vitamin E, reduced glutathione (GSH), and oxidized glutathione (GSSG) levels were altered. Similarly, the activities of total ATPases, Na+/K+-ATPase, Ca2+-ATPase, and Mg2+-ATPase were also decreased in the erythrocytes of diabetic rats. Administration of SGF to STZ-induced diabetic rats reduced blood glucose and glycosylated haemoglobin levels with increased levels of insulin and haemoglobin. Moreover, SGF reversed the protein and lipid peroxidation markers, osmotic fragility, membrane-bound ATPases activities, and antioxidant status in STZ-induced diabetic rats. These results suggest that SGF could provide a protective effect on diabetes by decreasing oxidative stress-associated diabetic complications.

Download Full-text

Maternal Urinary Metal and Metalloid Concentrations in Association with Oxidative Stress Biomarkers

Antioxidants ◽

10.3390/antiox10010114 ◽

2021 ◽

Vol 10 (1) ◽

pp. 114

Author(s):

Pahriya Ashrap ◽

Deborah J. Watkins ◽

Ginger L. Milne ◽

Kelly K. Ferguson ◽

Rita Loch-Caruso ◽

...

Keyword(s):

Oxidative Stress ◽

Prostaglandin F2α ◽

Urine Samples ◽

Oxidative Stress Marker ◽

Essential Metals ◽

Male Fetus ◽

Metal Concentrations ◽

Fetal Sex ◽

Wide Range ◽

And Oxidative Stress

Metal exposure has been associated with a wide range of adverse birth outcomes and oxidative stress is a leading hypothesis of the mechanism of action of metal toxicity. We assessed the relationship between maternal exposure to essential and non-essential metals and metalloids in pregnancy and oxidative stress markers, and sought to identify windows of vulnerability and effect modification by fetal sex. In our analysis of 215 women from the PROTECT birth cohort study, we measured 14 essential and non-essential metals in urine samples at three time points during pregnancy. The oxidative stress marker 8-iso-prostaglandin F2α (8-iso-PGF2α) and its metabolite 2,3-dinor-5,6-dihydro-15-15-F2t-IsoP, as well as prostaglandin F2α (PGF2α), were also measured in the same urine samples. Using linear mixed models, we examined the main effects of metals on markers of oxidative stress as well as the visit-specific and fetal sex-specific effects. After adjustment for covariates, we found that a few urinary metal concentrations, most notably cesium (Cs) and copper (Cu), were associated with higher 8-iso-PGF2α with effect estimates ranging from 7.3 to 14.9% for each interquartile range, increase in the metal concentration. The effect estimates were generally in the same direction at the three visits and a few were significant only among women carrying a male fetus. Our data show that higher urinary metal concentrations were associated with elevated biomarkers of oxidative stress. Our results also indicate a potential vulnerability of women carrying a male fetus.

Download Full-text

Eugenol attenuates concanavalin A-induced hepatitis through modulation of cytokine levels and inhibition of mitochondrial oxidative stress

Archives of Biological Sciences ◽

10.2298/abs190121016l ◽

2019 ◽

Vol 71 (2) ◽

pp. 339-346

Author(s):

Jing Liu ◽

Yidong Mao

Keyword(s):

Oxidative Stress ◽

Concanavalin A ◽

Hepatoprotective Activity ◽

Antioxidant Enzyme Activities ◽

Mitochondrial Oxidative Stress ◽

Immune Mediated ◽

Wide Range ◽

Cytokine Levels ◽

Glucose 6 Phosphate Dehydrogenase

Therapeutic management of hepatitis with conventional drugs alone worsens hepatic functioning in the long term because of sustained oxidative stress. Active compounds from several plant sources have been investigated to counteract this. Eugenol, a phytochemical abundant in various plants, is known for its wide range of pharmacological effects. There is a lacuna in the deeper understanding of its hepatoprotective activity at the molecular level. Our present study aimed to determine the effects of eugenol on the changes in antioxidant components, inflammatory cytokines and modulation of mitochondrial oxidative stress in immune-mediated hepatitis. We employed a model that mimics viral hepatitis using concanavalin A (ConA) to induce T-cell-mediated acute hepatitis. Eugenol increased (P<0.01) antioxidant enzyme activities, including reduced glutathione (GSH)-regenerating enzyme, glutathione reductase, and glucose-6-phosphate dehydrogenase. Its antiinflammatory and antifibrogenic effects were evident from the reduction (P<0.01) in interleukin and tumor necrosis factor levels. Eugenol was found to decrease mitochondrial oxidative stress, which was elevated in hepatitis. The hepatoprotective effects of eugenol were confirmed by histological findings. The current investigation shows that eugenol exerts a hepatoprotective effect through the modulation of different pathways which include restoration of mitochondrial oxidative stress. Eugenol could be a promising candidate for human hepatitis management, warranting preclinical studies.

Download Full-text

Exploration of the optimal strategy for dietary calcium intervention against the toxicity of liver and kidney induced by cadmium in mice: An in vivo diet intervention study

PLoS ONE ◽

10.1371/journal.pone.0250885 ◽

2021 ◽

Vol 16 (5) ◽

pp. e0250885

Author(s):

Zhaofang Chen ◽

Kexin Shi ◽

Wenjie Kuang ◽

Lei Huang

Keyword(s):

Oxidative Stress ◽

Dietary Intervention ◽

Essential Element ◽

Control Group ◽

Protective Effects ◽

Oxidative Stress Biomarkers ◽

Diet Intervention ◽

Stress Biomarkers ◽

Exposure Pathway ◽

Group 2

Cadmium (Cd) is a toxic non-essential element, while calcium (Ca) is an essential element with high chemical similarity to Cd. Dietary intake is the major Cd exposure pathway for non-smokers. A multi-concentration dietary intervention experiment was designed to explore the optimum concentration of Ca in diet with obvious protective effects against the toxicity of livers and kidneys induced by Cd in mice. The mice were divided into six groups with different concentrations of Cd and Ca in their food: control-group (no Cd or Ca), Ca-group (100 g/kg Ca, without Cd), Cd-group (2 mg/kg Cd, without Ca), CaL+Cd-group (2 mg/kg Cd, 2 g/kg Ca), CaM+Cd-group (2 mg/kg Cd, 20 g/kg Ca) and CaH+Cd-group (2 mg/kg Cd, 100 g/kg Ca). The organ indexes, oxidative stress biomarkers, lesions and Cd concentrations were detected after a 30-day exposure period. Results showed that serum Aspartate Aminotransferase (AST) level in CaH+Cd-group was significantly lower than that in Cd-group, while close to that in control-group. The contents of Serum Blood Urea Nitrogen (BUN) in different groups showed the same trend. Concentrations of all oxidative stress biomarkers (GSH-Px, SOD, CAT, GSH and MDA) in CaH+Cd-group were close to the normal levels of control-group while significantly different from those in Cd-group. The only exception was the Malondialdehyde (MDA) levels in kidneys. This study suggests that Ca plays a protective role in relieving the Cd-induced toxicity of livers and kidneys and a concentration of 100 g/kg for Ca in diet showed the best protective effects. These findings could provide a clue for further studies concerning human diet intervention for Cd control.

Download Full-text