Reduced Glutathione Activity Research Articles

Isolation and Characterization of Chitin Nanofibers from Calocybe indica and its Applications

In this study, chitin nanofibers are isolated from Calocybe indica (Milky White Mushroom), and they are further characterized using various analytical techniques such as UV-VIS, FTIR, TGA, Fe - SEM, and XRD. Antioxidant activity of the chitin nanofibers was studied by performing various assays such as DPPH, ABTS, H2O5 Scavenging Activity, Hydroxyl Radical Activity, Superoxide Assay, and Reduced Glutathione Activity. Isolated Chitin nanofibers were then chemically treated to form hydrogels. The hydrogels formed were further characterized.

In-vitro Cytoprotective Activity of Eichhornia crassipes Flowers Against Hydrogen Peroxideinduced Oxidative Stress in BRL 3A Rat Liver Cells

The aim of this study was to investigate the cytoprotective effect of ethanol extract of Eichhornia crassipes flowersand its fractions against hydrogen peroxide induced oxidative stress in BRL 3A liver cells. Powdered flowers of Eichhornia crassipeswere subjected to hot continuous extraction in soxhlet extractor using ethanol as solvent material. Initially, the solvent extracts were subjected to qualitative, quantitative analysis and assessed for in-vitro free radical scavenging activity and anti-oxidant activity. The ethanol extract was fractionated using benzene, chloroform and n-butanol. The crude ethanol extract and its fractions were evaluated for its potential cytoprotective effect against hydrogen peroxide (H2O2) induced oxidative stress in BRL 3A cell lines.Biochemical assays were carried out to determine the cytoprotective activity, including cell viability, lipid peroxidation by determining the formation of malondialdehyde, lactate dehydrogenase leakage into culture medium, the catalase activity and the content of reduced glutathione (GSH) in the cells. Exposure of BRL 3A to 2mM H2O2 reduced the cell viability, increased the malondialdehyde (MDA) level, increased the leakage of lactate dehydrogenase (LDH) and caused reduction in antioxidant activities. Pretreatment of cultured cells with crude ethanol extract of Eichhornia crassipes flowers and different solvent fractions at concentrations 0.01, 0.1, 1, 10, 100 μg/ml for 30 minutes before H2O2 exposure attenuated the oxidative injury in dose-dependent manner. It was observed that crude ethanol extract of Eichhornia crassipes flowers exhibited a strong cytoprotective by increasing cell viability, decreasing lipid peroxidation and LDH leakage. Further increase in catalase and reduced glutathione activity was noted in the cells pre-treated with ethanol extract of Eichhornia crassipes flowers. These findings suggest that ethanol extract of Eichhornia crassipes flowers has a strong cytoprotective activity against oxidative injury caused by reactive oxygen species.

Attenuating Effect of Vitamin E and Tinospora cordifolia on Bisphenol-A Induced Apoptosis in Goat Testis

During the present study effect of Vitamin E and Tinospora cordifolia on BPA induced goat (Capra hircus) testicular tissue was evaluated. Testicular tissue was exposed to varied concentrations of BPA, Vitamin E and Tinospora cordifolia in three experimental groups along with their specific control for 4 and 8hrs. In group I, the cultured tissue was exposed to three doses of Bisphenol-A viz. 0.01, 1.0 and 100 nM/ml. In group II, Vitamin E (0.1µM/ml) was supplemented along with BPA (0.01, 1.0, 100 nM/ml) and in group III Tinospora cordifolia extract (250 µg/ml) was added with BPA (0.01, 1.0, 100 nM/ml) in the culture media. With the increase in dose level as well as the exposure duration, the frequency of apoptotic cells increased significantly (p< 0.05), as revealed by acridine orange and methylene blue staining. BPA exposure also induced a decline in the antioxidant enzyme activity such as catalase, glutathione peroxidase and reduced glutathione. Vitamin E and Tinospora cordifolia resulted in a decrease in the percentage of apoptotic cells and an increase in levels of catalase, glutathione peroxidase and reduced glutathione activity was observed. Hence, it is concluded that BPA induced more damage at its higher concentration and the antioxidant Vitamin E and Tinospora cordifolia ameliorate the oxidative stress-induced changes, thereby suggesting the potential of Vitamin E and Tinospora cordifolia in counteracting the cellular damage induced by agents like BPA.

EFFECT OF THE THERAPEUTIC-PREVENTIVE COMPLEX ON THE PARAMETERS OF GLUTATHIONE SYSTEM AND GLUTATHIONE-DEPENDENT ENZYMES OF THE ORAL FLUID IN CHILDREN WITH CHRONIC CATARRHAL GINGIVITIS AND DIABETES MELLITUS

EFFECT OF THE THERAPEUTIC-PREVENTIVE COMPLEX ON THE PARAMETERS OF GLUTATHIONE SYSTEM AND GLUTATHIONE-DEPENDENT ENZYMES OF THE ORAL FLUID IN CHILDREN WITH CHRONIC CATARRHAL GINGIVITIS AND DIABETES MELLITUS

Alternative protein source: Acceptability of cow blood meal in place of fish meal assessed via growth, antioxidant enzymes functions and haematological response inClarias gariepinus(Burchell, 1822)

This study investigated the dietary substitution effect of fish meal (FM) with cow blood meal (CBM) on growth performance, feed utilization, haematology and functions of antioxidant enzymes in Clarias gariepinus. In the test diets, FM was substituted with CBM at 7% (CBM1), 17% (CBM2), 25% (CBM3) and 33% (CBM4) inclusions. Feeding trial lasted 51 days after which the biological assays were conducted. Fish fed 7% CBM recorded better growth performance (average body weight, relative growth rate and food conversion ratio), while 33% CBM fed fish performed poorly. Incorporation of CBM in fish had no substantial effect on packed cell volume and white blood cell contents. Additionally, red blood cell count of the fish fed CBM2 decreased markedly, relative to control. When 7% CBM dietary inclusion level was exceeded in experimental feed formulation (CBM 2, 3, 4), the activities the following antioxidant enzymes: superoxide dismutase, catalase and glutathione peroxidase declined considerably, while glutathione reductase and reduced glutathione activities elevated significantly. Malondialdehyde contents elevated prominently in CBM 2, 3 and 4 groups compared to CBM1 and the control. Dietary incorporation of CBM of more than 7% negatively affected growth, feed utilization, altered antioxidant enzymes functions and malondialdehyde levels in C. gariepinus.

Antioxidant and Cognitive Enhancing Activities of Sargassum ilicifolium and Padina tetrastromatica in Scopolamine Treated Mice

Sargassum ilicifolium (Turner) C. Agardh (SI) and Padina tetrastromatica (Hauck) (PT) are tropical and sub-tropical brown algae, found in the coastal region of India. In the present study, the cognitive enhancing activity of chloroform and ethanol extract of SI and PT (CSI, ESI & CPT, EPT) was investigated in scopolamine- induced amnesic mice using the Passive avoidance (PA) test. In addition, the effect on brain oxidative enzymes and acetylcholinesterase (AChE) was also evaluated using a spectrophotometer. The results of this study indicated that CSI (600 mg/kg), ESI (600 mg/kg), as well as CPT (600 mg/kg), significantly increased Step-Down Latency compared to scopolamine treated group, indicated that, CSI, ESI and CPT significantly (p < 0.01) reversed memory deficit produced by scopolamine. Further, administration of CSI (600 mg/kg), ESI (600 mg/kg), as well as CPT (600 mg/kg), produced a significant (p < 0.01) fall in Malondialdehyde and increased in Reduced glutathione activity, indicated that CSI, ESI, and CPT exert a protective effect against oxidative damage induced by scopolamine. Also, it was found that, CSI (600 mg/kg), ESI (600 mg/kg) and CPT (600 mg/kg) significantly (p < 0.05) inhibit AChE activity. These findings resemble the effect of the standard anti-amnesic drug Piracetam. In conclusion, chloroform and ethanol extract of SI and PT shows significant cognitive-enhancing activities by the inhibition enzyme AChE and by the regulation of the oxidative enzymes in scopolamine-induced amnesic mice. However, further research is essential to explore the exact mechanism underlying this activity.

Cadmium induced oxystress alters Nrf2-Keap1 signaling and triggers apoptosis in piscine head kidney macrophages

Cadmium (Cd) with no known functional role in any life-form has myriad of harmful effects. The present study was designed to elucidate the mechanism of Cd-induced oxystress generation and its impact on antioxidant and apoptosis signaling pathways in head kidney macrophage (HKM) of Channa punctatus Bloch. Fish were sampled and acclimatized with one group treated with cadmium chloride (CdCl2) (1.96 mg/L) and another as untreated control group, both kept under observation for 7 days. Exposure to Cd caused ultrastructural changes along with reduced head kidney somatic index (HKSI). Significantly increased levels of reactive oxygen species (ROS), respiratory burst activity, lipid peroxidation, DNA fragmentation and superoxide dismutase were found in the HKM from the treated group as compared to control. In contrast, antioxidant enzymes like catalase and reduced glutathione activity decreased in the Cd exposed group. The suppressed antioxidant activity was further confirmed and corroborated from the altered expression of Kelch-like ECH-associated protein 1 (Keap1) and nuclear factor erythroid 2-related factor 2 (Nrf2) genes, the major player of antioxidant pathway. Cd induced alteration in Nrf2-Keap1 signaling pathway was also validated by the diminished levels of Nrf2 dependent expression of protein like heme oxygenase-1 (HO-1). The flow cytometry analysis supported the event of apoptosis in Cd exposed group as compared to control, which was further confirmed by the upregulated expression of caspase-3, caspase-8, caspase-9, TNF-α and p53 genes from the real-time gene expression study. In addition, altered protein level of cytochrome C validates the incidence of apoptosis. Altogether, our results demonstrate that exposure to Cd caused oxidative stress in HKM of Channa punctatus Bloch. by compromising the antioxidant enzyme activities via the down regulation of expression of genes related to antioxidant signaling pathway besides encouraging apoptosis via both mitochondrial and death receptor pathway.

Inhibition of thrombospondin-1 reduces glutathione activity and worsens acute liver injury during acetaminophen hepatotoxicity in mice

Acetaminophen (N-Acetyl-p-Aminophenol or APAP)-induced hepatotoxicity is the most common cause of acute liver failure in the United States and Western Europe. Previous studies have shown that TGFβ1 is elevated during APAP-induced hepatotoxicity and promotes liver injury by reducing liver regeneration while inducing hepatocyte senescence. At this time, little is known about the role of proteins that activate latent TGFβ1 and their effects during APAP-induced hepatotoxicity. Thrombospondin-1 (TSP1) is a homotrimeric protein that can not only activate latent TGFβ1 but can also interact with other proteins including Nrf2 to induce antioxidant signaling. The aim of the current study was to assess the role of thrombospondin-1 (TSP1) in both TGFβ1 activation and its contribution to APAP-induced liver injury. C57Bl/6 mice or TSP1 null mice (TSP1−/−) were administered 300 mg/kg or 600 mg/kg of APAP. TGFβ1 signaling, TSP1 expression, measures of hepatic injury, Nrf2 expression, measures of oxidative/nitrosative stress and GSH metabolism were assessed. The expression of TGFβ1, TSP1 and phosphorylation of SMAD proteins increased in APAP-treated mice compared to controls. TSP1−/− mice had reduced TGFβ1 expression and phosphorylation of SMAD proteins but increased liver injury. Hepatocyte cell death was increased in TSP1−/− mice and this was associated with decreased Nrf2 activity, decreased GSH levels and increased oxidative stress in comparison to wild-type C57Bl/6 mice. Together, these data demonstrate that elimination of TSP1 protein in APAP-treated mice reduces TGFβ1 signaling but leads to increased liver injury by reducing Nrf2 expression and GSH activity, ultimately resulting in increased cell death.

Echinacea polysaccharide attenuates lipopolysaccharide‑induced acute kidney injury via inhibiting inflammation, oxidative stress and the MAPK signaling pathway

Acute kidney injury (AKI) is often accompanied by inflammation. Echinacea polysaccharide (EP) is an active ingredient that has been demonstrated to possess anti-oxidative, anti-inflammatory, antimicrobial and immunomodulatory functions. However, the role of EP in AKI has not been examined. The present study investigated the effects of EP on lipopolysaccharide (LPS)-induced AKI. Western blotting, immunohistochemistry and immunofluorescence analyses were performed to detect protein expression levels. Administration of EP significantly attenuated LPS-induced renal tissue injury, along with a decrease in blood urea nitrogen and creatinine levels. EP decreased the levels of inducible nitric oxide synthase and cyclo-oxygenase-2 in LPS-treated mice. Furthermore, LPS-induced inflammation was inhibited by EP in renal tissues and HBZY-1 cells, as demonstrated by the downregulation of tumor necrosis factor-α, interleukin (IL)-1β, IL-6, nitric oxide and prostaglandin E2 levels. Similarly, EP administration decreased oxidative stress (OS) via decreasing reactive oxygen species, malondialdehyde and oxidized glutathione levels, and increasing superoxide dismutase, catalase, glutathione reductase and reduced glutathione activity. Notably, EP induced a marked decrease in the expression levels of phospho-extracellular signal-regulated protein kinase (p-ERK), phospho-c-Jun N-terminal kinase (p-JNK) and p-p38 in vivo and in vitro. In addition, in LPS-treated HBZY-1 cells, EP enhanced cell viability and inhibited nuclear translocation of p-ERK, p-JNK and p-p38. Overall, the present findings demonstrated that EP alleviated LPS-induced AKI via the suppression of inflammation, OS and the mitogen-activated protein kinase signaling pathway, providing insight into potential avenues for the treatment of AKI.

Hormone-Independent Mouse Mammary Adenocarcinomas with Different Metastatic Potential Exhibit Different Metabolic Signatures

The metabolic characteristics of metastatic and non-metastatic breast carcinomas remain poorly studied. In this work, untargeted Nuclear Magnetic Resonance (NMR) metabolomics was used to compare two medroxyprogesterone acetate (MPA)-induced mammary carcinomas lines with different metastatic abilities. Different metabolic signatures distinguished the non-metastatic (59-2-HI) and the metastatic (C7-2-HI) lines, with glucose, amino acid metabolism, nucleotide metabolism and lipid metabolism as the major affected pathways. Non-metastatic tumours appeared to be characterised by: (a) reduced glycolysis and tricarboxylic acid cycle (TCA) activities, possibly resulting in slower NADH biosynthesis and reduced mitochondrial transport chain activity and ATP synthesis; (b) glutamate accumulation possibly related to reduced glutathione activity and reduced mTORC1 activity; and (c) a clear shift to lower phosphoscholine/glycerophosphocholine ratios and sphingomyelin levels. Within each tumour line, metabolic profiles also differed significantly between tumours (i.e., mice). Metastatic tumours exhibited marked inter-tumour changes in polar compounds, some suggesting different glycolytic capacities. Such tumours also showed larger intra-tumour variations in metabolites involved in nucleotide and cholesterol/fatty acid metabolism, in tandem with less changes in TCA and phospholipid metabolism, compared to non-metastatic tumours. This study shows the valuable contribution of untargeted NMR metabolomics to characterise tumour metabolism, thus opening enticing opportunities to find metabolic markers related to metastatic ability in endocrine breast cancer.

Blood Oxidative Stress Modulates Alveolar Bone Loss in Chronically Stressed Rats

We aimed to investigate the effects of chronic stress (CS) on experimental periodontitis (EP) in rats. For this, 28 Wistar rats were divided into four groups: control, ligature-induced experimental periodontitis (EP), chronic stress (CS; by physical restraint model) and CS+EP (association of chronic stress and ligature-induced periodontitis). The experimental period lasted 30 days, including exposure to CS every day and ligature was performed on the 15th experimental day. After 30 days, the animals were submitted to the behavioral test of the elevated plus maze (EPM). Next, rats were euthanized for blood and mandible collection in order to evaluate the oxidative biochemistry (by nitric oxide (NO), reduced-glutathione activity (GSH), and thiobarbituric acid reactive substance levels (TBARS)) and alveolar bone characterization (by morphometric, micro-CT, and immunohistochemistry), respectively. The behavioral parameters evaluated in EPM indicated higher anxiogenic activity in the CS and CS+EP, groups, which is a behavioral reflex of CS. The results showed that CS was able to change the blood oxidative biochemistry in CS and CS+EP groups, decrease GSH activity in the blood, and increase the NO and TBARS concentrations. Thus, CS induces oxidative blood imbalance, which can potentialize or generate morphological, structural, and metabolic damages to the alveolar bone.

Polysaccharides from Opuntia milpa alta alleviate alloxan-induced INS-1 cells apoptosis via reducing oxidative stress and upregulating Nrf2 expression

The incidence and progression of type 2 diabetes are closely related to pancreatic β-cell damage. Oxidative stress may be one of the key factors contributing to β-cell apoptosis. Opuntia milpa alta polysaccharides (MAPs) are water-soluble macromolecular polysaccharides that have antidiabetic effects in vivo. Therefore, we hypothesized that MAPs might effectively prevent β-cell apoptosis via the inhibition of oxidative damages. In this study, INS-1 cells were exposed to alloxan with different concentrations of MAPs in vitro, and the cell viability, oxidative enzyme activities, nitric oxide production, reactive oxygen species production, apoptosis, and the expression of proteins in the antioxidant nucleus transcription factor NF-E2–related factor 2 (Nrf2) pathway and proteins related to apoptosis were measured to assess oxidative stress responses and apoptosis. The results indicated that INS-1 cell viabilities and superoxide dismutase and reduced glutathione activities were significantly restored, whereas lactate dehydrogenase releases and reactive oxygen species, nitric oxide, and malondialdehyde levels were greatly decreased after MAPs treatment. We found that MAPs could attenuate alloxan-induced apoptosis by increasing the expression of Bcl-2 and decreasing the expression of Bax and the activities of caspase-3 and caspase-9. The results of Western blot revealed that MAPs suppressed the expression of cleaved caspase-3 and cleaved PARP and upregulated the expression of nucleus Nrf2 and its downstream protein. These findings indicated that MAPs could alleviate alloxan-induced β-cell apoptosis by reducing oxidative stress and upregulating Nrf2 expression.

Control of doxorubicin-induced, reactive oxygen-related apoptosis by glutathione peroxidase 1 in cardiac fibroblasts

Reactive oxygen formation plays a mechanistic role in the cardiotoxicity of doxorubicin, a chemotherapeutic agent that remains an important component of treatment programs for breast cancer and hematopoietic malignancies. To examine the role of doxorubicin-induced reactive oxygen species (ROS) in drug-related cardiac apoptosis, murine embryonic fibroblast cell lines were derived from the hearts of glutathione peroxidase 1 (Gpx-1) knockout mice. Cells from homozygous Gpx-1 knockout mice and parental animals were propagated with (Se+) and without (Se-) 100 nM sodium selenite. Activity levels of the peroxide detoxifying selenoprotein glutathione peroxidase (GSHPx) were marginally detectable (<1.6 nmol/min/mg) in fibroblasts from homozygous knockout animals whether or not cells were supplemented with selenium. GSHPx activity in Se- cells from parental murine fibroblasts was also <1.6 nmol/min/mg, whereas GSHPx levels in Se+ parental murine fibroblasts were 12.9 ± 2.7 nmol/min/mg (mean ± SE; P < 0.05). Catalase, superoxide dismutase, glutathione reductase, glutathione S-transferase, glucose 6-phosphate dehydrogenase, and reduced glutathione activities did not differ amongst the four cell lines. Reactive oxygen production increased from 908 ± 122 (arbitrary units) for untreated control cells to 1668 ± 54 following exposure to 1 μM doxorubicin for 24 h in parental fibroblasts not supplemented with selenium (P < 0.03); reactive oxygen formation in doxorubicin-treated parental fibroblasts propagated in selenium was 996 ± 69 (P = not significant compared to untreated control cells). Reactive oxygen levels in homozygous Gpx-1 knockout fibroblasts, irrespective of selenium supplementation status, were increased and equivalent to that in selenium deficient wild type fibroblasts. When cardiac fibroblasts were exposed to doxorubicin (0.05 μM) for 96 h and examined for cell cycle alterations by flow cytometry, and apoptosis by TUNEL assay, marked G2 arrest and TUNEL positivity were observed in knockout fibroblasts in the presence or absence of supplemental selenium, and in parental fibroblasts propagated without selenium. Parental fibroblasts propagated with selenium and exposed to the same concentration of doxorubicin demonstrated modest TUNEL positivity and substantially diminished amounts of low molecular weight DNA. These results were replicated in cardiac fibroblasts exposed to doxorubicin (1–2 μM) for 2 h (to mimic clinical drug dosing schedules) and examined 96 h following initiation of drug exposure. Doxorubicin uptake in cardiac fibroblasts was similar irrespective of the mRNA expression level or activity of GSHPx. These experiments suggest that the intracellular levels of doxorubicin-induced reactive oxygen species (ROS) are modulated by GSHPx and play an important role in doxorubicin-related apoptosis and altered cell cycle progression in murine cardiac fibroblasts.

Culture of goat preantral follicles in situ associated with mesenchymal stem cell from bone marrow.

This study aims to develop an in vitro co-culture system of in situ goat preantral follicles with bone marrow-derived mesenchymal stem cells (BM-MSC), evaluating the influence of these cells on follicular growth, rate of activation and morphologically normal follicles. Fragments of ovarian cortex were cultured for 1 or 7 days in the presence of BM-MSC (BM-MSC+) and absence of BM-MSC (BM-MSC-). Histological sections of the fragments were analysed and data were obtained regarding morphological classification, survival rate of morphologically normal follicles and rate of follicular activation. Culture medium on days 1 and 7 was also sampled for nitrite concentration and reduced glutathione activity. There was a reduction (P < 0.05) in the percentage of morphologically normal follicles in the BM-MSC+ compared with the fresh control only on the seventh day of culture. When comparing treatments, on the seventh day of culture, a higher rate of morphologically normal preantral follicles was observed in BM-MSC+ (P < 0.05). In both treatments, primordial and developing follicle rates were similar to the fresh control (P > 0.05). When comparing treatments with each other, as well as with the fresh control, no differences were observed in follicular diameter (P > 0.05) or nitrite concentration (P > 0.05). The concentration of reduced glutathione was lower on the seventh day of co-culture in both treatments (P < 0.05). In conclusion, co-culture had no influence on follicular or oocyte development. However, it was critical to maintain the survival of preantral follicles during 7 days of culture.

Neuroprotective Effects of Mitochondria-Targeted Quercetin Against Rotenone-Induced Oxidative Damage in Cerebellum of Mice

Mitochondrial dysfunction leads to various types of metabolic impairments, including decreased ATP formation, diminished calcium buffering, gathering of metabolic intermediates and amplified production reactive oxygen species and reactive nitrogen species. Rotenone is a strong inhibitor of complex I and causes mitochondrial dysfunction, leads to motor impairment, metabolic disorder and cellular damage. Quercetin is a strong antioxidant and neuroprotective against neurodegenerative diseases, but its efficacy is limited because it does not gather into the mitochondria. Therefore, mitochondrially targeted antioxidants have to be developed by conjugating with lipophilic cation which can freely cross through the mitochondrial membrane and protects mitochondrial injury. This study investigated the protective effect of quercetin and mitochondrial-targeted quercetin (MTQ) in rotenone-induced cerebellar toxicity in mice. Treatment of rotenone (3 mg/kg b.w., p.o for 60 days) in mice significantly increases in the levels of lipid peroxidation, nitric oxide and decrease in the activity of AChE, reduced glutathione, superoxide dismutase and catalase were observed in mice compared to controls. Co-treatment of quercetin and MTQ (30mg/kg b.w., p.o) along with rotenone significantly increased AChE activity and protected against rotenone-induced enhanced oxidative stress. Histological study of cerebellum exhibited necrosis of Purkinje cells as revealed by irregular, damaged cells and perineuronal vacuolation in rotenone-treated mice. Co-treatment of quercetin and MTQ along with rotenone showed protection against rotenone-induced cellular damage in these cells. The results exhibit that both quercetin and MTQ showed a protective effect against rotenone-induced cerebellar toxicity in mice and MTQ is more effectively showed protection than quercetin.

Effects of Moringa oleifera extracts and monensin on performance of growing rabbits

This study was designed to assess the effects of Moringa oleifera (moringa) leaf ethanolic extract (MLEE), moringa root ethanolic extract (MREE), and ionophore antibiotic monensin on growth performance, hematological variables, blood plasma metabolites and antioxidant indicators, digestibility, and cecal fermentation of growing rabbits. A total of 96 growing rabbits weaned at 35 d of age were randomly assigned to 4 treatments with 12 male and 12 female rabbits/treatment. The first treatment was the control (no additives), the second treatment was a basal diet containing 10 mg monensin/kg dry matter (DM), and the third and fourth treatments were MLEE and MREE, respectively, at concentration of 250 mg/L drinking water. From 35 to 77 d of age, the rabbits were housed in groups (8 cages/treatment, 3 rabbits/cage), and growth performance variables including body weight (BW), feed consumption, BW gain, and feed conversion ratio were recorded. From 78 to 93 d of age, after the end of the growth performance trial, the rabbits were housed individually. At 87 d of age, blood samples were collected from 10 rabbits (5 males and 5 females) that were selected randomly to determine hematological variables and blood plasma metabolites and antioxidant indicators. From 87 to 93 d of age, 8 male rabbits/treatment were selected randomly to determine digestibility, N balance, and cecal fermentation activity. The major chemical compounds in MLEE were α-linolenic acid, glycerine, ascorbic acid, and diethyl phthalate, whereas ascorbic acid, S-phenylmercapturic acid, 2-myristynoyl pantetheine, and 8,11,14-docosatrienoic acid, methyl ester were major compounds in MREE. Both the MLEE and MREE treatments improved (P < 0.05) final BW and overall feed conversion ratios compared to the monensin and control treatments. From d 64 to 77 of age, the monensin treatment decreased (P < 0.05) feed consumption compared to the other treatments. None of the treatments affected hematological variables, but the monensin, MLEE, and MREE treatments increased (P < 0.05) plasma albumin concentration. The monensin and MREE treatments decreased (P < 0.05) plasma globulin concentration compared to the MLEE and control treatments. Compared to the control, the monensin, MLEE, and MREE treatments increased (P < 0.05) plasma total antioxidant capacity by 66.17% but decreased (P < 0.05) both the plasma malondialdehyde concentration by 24.96% and reduced glutathione activity by 25.96%. The MLEE treatment increased (P < 0.05) the apparent digestibility of acid detergent fiber (6.49%) and hemicellulose (13.53%) compared to the other treatments. The MLEE and MREE treatments increased (P < 0.05) apparent cellulose digestibility and body N retention compared to the monensin and control treatments. The lowest (P < 0.05) cecal total volatile fatty acid concentration was observed with the monensin treatment, while the greatest (P < 0.05) was with the MLEE treatment. Compared to the control, the monensin and MLEE treatments decreased the molar proportions of butyrate (72.20 and 31.10%, respectively; P < 0.05) and increased the molar proportions of propionate (140.70 and 67.80%, respectively; P < 0.05). In conclusion, MLEE or MREE could be used at concentration of 250 mg/L drinking water to promote growth of weaned rabbits.

Evaluation of the effects of Cyclotrichium niveum on brain acetylcholinesterase activity and oxidative stress in male rats orally exposed to lead acetate

Cyclotrichium niveum is an endemic plant for Turkey and it appears to have in vitro antioxidant and acetylcholinesterase inhibition properties. To the best of our knowledge, there has been no study on the in vivo effects of this plant. Therefore, the purpose of this study was to evaluate the effects of C. niveum on lead (Pb)-acetate-induced potential alterations in brain acetylcholinesterase activity, as well as oxidative stress in male rats. The rats were randomly assigned to control, Pb-acetate, C. niveum and Pb-acetate+ C. niveum groups. Pb-acetate was provided in drinking water (500 ppm), and C. niveum was administered via orogastric gavage (4 ml/kg) for 30 days. The acetylcholinesterase activity in the brain significantly decreased only in the Pb-acetate group. The malondialdehyde level significantly increased, and the reduced glutathione activity decreased in the Pb-acetate group. The reduced glutathione and glutathione-S-transferase activities of the C. niveum group were higher than the control group. No Pb was detected on a ppb level in the brain tissue of the control and C. niveum groups, while it was detected in the brains of the rats in the Pb-acetate and Pb-acetate+ C. niveum groups (185+8.98 ppb and 206+56.65 ppb, respectively). The data collected in this study suggested that C. niveum may reduce inhibition of brain AChE activity and oxidative stress against Pb-acetate-induced alterations in the brain of male rats.

Impact of Smoking and Alcohol Consumption on Oxidative Status in Male Infertility and Sperm Quality

The most common unhealthy lifestyle factors like cigarette smoking and drinking alcohol have controversial reports on how these impact male fertility. The present study assessed the potential effects of these habits on sperm quality, male reproductive hormones, and blood plasma oxidative profile in 133 infertile men with 124 fertile, healthy controls. Among the participants, 28 (10.8 %), 29 (11.2 %), 33 (12.8 %), 34 (13.2 %) fertile men were non-alcoholics and non-smokers (total abstainers), smokers, alcohol drinkers, and smokers plus alcohol drinkers, respectively. On the other hand, 32 (12.4 %), 30 (11.6 %), 34 (13.2 %), 37 (14.3 %) infertile men were total abstainers, smokers, alcohol drinkers, and smokers plus alcohol drinkers, respectively. The conventional sperm parameters and reproductive hormone levels were found to be significantly different in the subsets of infertile men than those of fertile men (p<0.001). In these subsets of infertile men, blood plasma malondialdehyde, nitric oxide concentrations were significantly higher and superoxide dismutase, reduced glutathione activities were significantly lower when compared to fertile men and infertile men total abstainers group (p<0.001). In infertile subjects, particularly smoking-alcohol drinking group was more affected than only smoking or alcohol drinking groups. Furthermore, these oxidative markers were correlated with sperm concentration, motility, and morphology, except nitric oxide concentration, which was only associated with sperm motility. These findings highlighted that blood plasma antioxidants are as efficient as seminal plasma antioxidants in male fertility evaluation.

Hydrogen peroxide-induced oxidative stress, acetylcholinesterase inhibition, and mediated brain injury attenuated by Thymus algeriensis.

The aim of the current study was to evaluate acetylcholinesterase (AChE) inhibition, antioxidant enzyme activities, and malondialdehyde (MDA) levels induced by hydrophobic fractions of Thymus algeriensis (HFTS) growing in Tunisia. The results showed that hydrogen peroxide (H2O2), an oxidative stress inducer, acts by decreasing the body mass and brain mass of rats. Moreover, we found higher MDA levels in the group treated with H2O2 (P < 0.05) and a significantly lower activity of catalase, glutathione peroxidase, glutathione S-transferase, and superoxide dismutase, as well as a reduction in reduced glutathione activity in the brain tissues of H2O2-treated rats when compared with those of the control group (P < 0.05); however, rats that received HFTS with H2O2 experienced a decrease in MDA levels in the brain. In contrast, HFTS demonstrated neuroprotective effects in rat brain. Overall, exposure to HFTS prior to H2O2 induced a marked dose-dependent increase in reactive oxygen species scavenger levels (P < 0.05) accompanied by a statistically significant decrease in MDA levels (P < 0.05) when compared with no exposure. Notably, the activity of AChE was affected by exposure to natural compounds; levels were significantly lower in HFTS-treated rats and in those treated with the combination of HFTS and a low or high dose of H2O2. Furthermore, histopathological analysis showed that brain injuries occurred with high doses of H2O2 administered alone or with a low dose of HFTS, whereas a high dose of essential oil markedly alleviated neurone degeneration. The results suggest that HFTS alleviates neuroinflammation by acting as an AChE inhibitor and attenuates H2O2-induced brain toxicity.

Evaluation of the rivastigmine role against botulinum toxin-A-induced osteoporosis in albino rats: A biochemical, histological, and immunohistochemical study.

The present study aimed to evaluate the role of rivastigmine against the effect of a single unilateral botulinum toxin-A (BTX-A) injection on the bone and bone marrow of adult albino rats 4 weeks after injection. Twenty-four Wistar albino rats were divided into four equal groups: group I, which received distilled water; group II, which received rivastigmine (0.3 mg/kg daily, intraperitoneally for 4 weeks); group III, which received BTX-A (4 IU in 0.2 mL physiological saline) single dose, intramuscularly; and group IV, which received BTX-A + rivastigmine. The results revealed that BTX-A induced a significant decrease in the calcium level with a significant increase in the phosphorus, alkaline phosphatase, C-reactive protein, and tumor necrosis factor α levels in serum. Furthermore, a significant increase in malondialdehyde with a significant decrease in reduced glutathione activities in both bone and bone marrow. Histologically, a distortion and thinning out of the compact bone and trabeculae of cancellous bone of the rat femur in the BTX-A group with an increase in adipocytes in adjacent bone marrow were detected. Immunohistochemically, Cluster of Differentiation 68 (CD68) showed a significant increase in both osteoclasts and bone marrow macrophage. Rivastigmine treatment could relieve the toxic effects induced by BTX-A. In conclusion, rivastigmine has a protective effect against the hazardous effects of BTX-A on bone and bone marrow.