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Premature aging in behavior and immune functions in tyrosine hydroxylase haploinsufficient female mice. a longitudinal study.

Aging is accompanied by impairment in the nervous, immune, and endocrine systems as well as in neuroimmunoendocrine communication. In this context, there is an age-related alteration of the physiological response to acute stress, which is modulated by catecholamine (CA), final products of the sympathetic-adreno-medullary axis. The involvement of CA in essential functions of the nervous system is consistent with the neuropsychological deficits found in mice with haploinsufficiency (hemizygous; HZ) of tyrosine hydroxylase (TH) enzyme (TH-HZ). However, other possible alterations in regulatory systems have not been studied in these animals. The aim of the present work was to analyze whether adult TH-HZ female mice presented the impairment of behavioral traits and immunological responses that occurs with aging and whether they had affected their mean lifespan. ICR-CD1 female TH-HZ and wild type (WT) mice were used in a longitudinal study. Behavioral tests were performed on adult and old mice in order to evaluate their sensorimotor abilities and exploratory capacity, as well as anxiety-like behaviors. At the ages of 2±1, 4±1, 9±1, 13±1 and 20±1 months, peritoneal leukocytes were extracted and several immune functions were assessed (phagocytic capacity, Natural Killer (NK) cytotoxicity, and lymphoproliferative response to lipopolysaccharide (LPS) and concanavalin A (ConA)). In addition, several oxidative stress parameters (catalase, glutathione reductase and glutathione peroxidase activities, and reduced glutathione (GSH) concentrations as antioxidant compounds as well as xanthine oxidase activity, oxidized glutathione (GSSG) concentrations, and GSSG/GSH ratio as oxidants) were analyzed. As inflammatory stress parameters TNF-alpha and IL-10 concentrations, and TNF-alpha/IL-10 ratios as inflammatory/anti-inflammatory markers, were measured. Animals were maintained in standard conditions until their natural death. The results indicate that adult TH-HZ mice presented worse sensorimotor abilities and exploratory capacity than their WT littermates as well as greater anxiety-like behaviors. With regards to the immune system, adult TH-HZ animals exhibited lower values of phagocytic capacity, NK cytotoxicity, and lymphoproliferative response to LPS and ConA than WT mice. Moreover, immune cells of TH-HZ mice showed higher oxidative and inflammatory stress than those of WT animals. Although these differences between TH-HZ and WT, in general, decreased with aging, this premature immunosenescence and impairment of behavior of TH-HZ mice was accompanied by a shorter mean lifespan in comparison to WT counterparts. In conclusion, haploinsufficiency of th gene in female mice appears to provoke premature aging of the regulatory systems affecting mean lifespan.

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Deficiency of dietary pyridoxine disturbed the intestinal physical barrier function of young grass carp (Ctenopharyngodon idella).

The aim of this study was to assess the effects of dietary pyridoxine (PN) deficiency on intestinal antioxidant capacity, cell apoptosis and intercellular tight junction in young grass carp (Ctenopharyngodon idella). A total of 540 young grass carp (231.85 ± 0.63 g) were fed six diets containing graded levels of PN (0.12-7.48 mg/kg diet) for 10 weeks. At the end of the feeding trial, the fish were challenged with Aeromonas hydrophila for 2 weeks. The results showed that compared with the optimal PN level, PN deficiency (1) increased the contents of reactive oxygen species (ROS), malondialdehyde (MDA) and protein carbonyl (PC), decreased the activities and mRNA levels of antioxidant enzymes such as copper, zinc superoxide dismutase (CuZnSOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and glutathione reductase (GR) (P < .05); (2) up-regulated the mRNA levels of cysteinyl aspartic acid-protease-3 (caspase-3), caspase-7, caspase-8, caspase-9, Bcl-2 associated X protein (Bax), apoptotic protease activating factor-1 (Apaf-1) and Fas ligand (FasL), and down-regulated the mRNA levels of inhibitor of apoptosis proteins (IAP), B-cell lymphoma protein-2 (Bcl-2) and myeloid cell leukaemia-1 (Mcl-1) (P < .05); (3) down-regulated the mRNA levels of ZO-1, occludin [only in middle intestine (MI)], claudin-b, claudin-c, claudin-f, claudin-3c, claudin-7a, claudin-7b and claudin-11, and up-regulated the mRNA levels of claudin-12 and claudin-15a (P < .05), which might be partly linked to Kelch-like-ECH-associated protein 1a (Keap1a)/NF-E2-related factor 2 (Nrf2), p38 mitogen-activated protein kinase (p38MAPK) and myosin light chain kinase (MLCK) signalling in the intestines of fish. However, the activities and mRNA levels of MnSOD, the mRNA levels of Keap1b, c-Jun N-terminal protein kinase (JNK) and claudin-15b in three intestinal segments, and the mRNA levels of occludin in the proximal intestine (PI) and distal intestine (DI) were not affected by graded levels of PN. These data indicate that PN deficiency could disturb the intestinal physical barrier function of fish. Additionally, based on the quadratic regression analysis for MDA content and GST activity, the dietary PN requirements for young grass carp were estimated as 4.85 and 5.02 mg/kg diet, respectively.

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Selenium regulation of selenoprotein enzyme activity and transcripts in a pilot study with Founder strains from the Collaborative Cross.

Rodents and humans have 24-25 selenoproteins, and these proteins contain the 21st amino acid, selenocysteine, incorporated co-translationally into the peptide backbone in a series of reactions dependent on at least 6 unique gene products. In selenium (Se) deficiency, there is differential regulation of selenoprotein expression, whereby levels of some selenoproteins and their transcripts decrease dramatically in Se deficiency, but other selenoprotein transcripts are spared this decrease; the underlying mechanism, however, is not fully understood. To begin explore the genetic basis for this variation in regulation by Se status in a pilot study, we fed Se-deficient or Se-adequate diets (0.005 or 0.2 μg Se/g, respectively) for eight weeks to the eight Founder strains of the Collaborative Cross. We found rather uniform expression of selenoenzyme activity for glutathione peroxidase (Gpx) 3 in plasma, Gpx1 in red blood cells, and Gpx1, Gpx4, and thioredoxin reductase in liver. In Founder mice, Se deficiency decreased each of these activities to a similar extent. Regulation of selenoprotein transcript expression by Se status was also globally retained intact, with dramatic down-regulation of Gpx1, Selenow, and Selenoh transcripts in all 8 strains of Founder mice. These results indicate that differential regulation of selenoprotein expression by Se status is an essential aspect of Se metabolism and selenoprotein function. A few lone differences in Se regulation were observed for individual selenoproteins in this pilot study, but these differences did not single-out one strain or one selenoprotein that consistently had unique Se regulation of selenoprotein expression. These differences should be affirmed in larger studies; use of the Diversity Outbred and Collaborative Cross strains may help to better define the functions of these selenoproteins.

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Protective effect of flavonoids from Cyclocarya paliurus leaves against carbon tetrachloride-induced acute liver injury in mice.

Cyclocarya paliurus (Batal.) Iljinskaja (C. paliurus), known locally as 'sweet tea tree', is commonly cultivated in China. Flavonoids from Cyclocarya paliurus (Batal.) Iljinskaja (FC) is reported to exhibit multiple biological effects, including anti-inflammatory, anti-oxidant and anti-diabetic activities. However, their influence on carbon tetrachloride (CCl4)-induced acute liver injury remains unclear. This study was designed to investigate the hepatoprotective effect of total flavonoids from C. paliurus leaves. Results revealed that flavonoids from C. paliurus significantly decreased CCl4-induced elevation of activities of aspartate transaminase (AST), alanine transaminase (ALT) and superoxide dismutase (SOD) as well as the level of malondialdehyde (MDA), and markedly increased the levels of SOD, total antioxidant capacity (T-AOC) and glutathione peroxidase (GSH-Px) compared with the model group. Structures of mainly compounds were elucidated by nuclear magnetic resonance (NMR), mass spectrometry (MS) spectroscopic and chemical analyses. This study clearly shows that flavonoids from C. paliurus exert a potent protective effect against CCl4-induced acute liver injury in mice. Its hepatoprotective effect appears to be closely associated with its antioxidant activity. The results indicated that flavonoids from C. paliurus leaves could be considered as a potent food supplement in the prevention of acute liver injury.

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Altered redox state modulates endothelial KCa2.3 and KCa3.1 levels in normal pregnancy and preeclampsia.

Altered redox state has been related to the development of normal pregnancy (NP) and preeclampsia (PE). Endothelial KCa2.3 and KCa3.1 (KCas) play an important role in vasodilation, and KCas levels are affected by oxidative stress. We investigated the mechanisms of oxidative stress-mediated KCas expression modulation during NP and PE.

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Effects of Berberine chloride on the liver of streptozotocin-induced diabetes in albino Wistar rats.

The goal of the present study is to evaluate the effect of Berberine chloride (BC) on the liver of streptozotocin (STZ) induced diabetic rat. Diabetic rats were treated with BC (50 mg/kg b.w) or glibenclamide (6 mg/kg b.w), daily for 45 days. After BC treatment in diabetic rats, there was a significant (P < 0.05) decline in the levels of hepatic markers, lipid peroxidation markers such as lipid hydroperoxides (LOOH) and thiobarbituric acid reactive substances (TBARS), and pro-inflammatory mediators like tumor necrosis factor-alpha (TNF-α), phosphorylated nuclear factor kappa-B-p65 (phospho-NF-κB p65), cyclooxygenase (COX-2), nitric oxide synthase (iNOS) as well as pro-apoptotic mediators such as Bax and cytochrome c. A significant (P < 0.05) increase in hexokinase, glucose-6-phosphate dehydrogenase, enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), and non-enzymatic antioxidants such as glutathione (GSH), vitamin E and vitamin C, as well as anti-apoptotic protein Bcl-2 were observed in the liver of BC treated diabetic rats. Thus, from these findings, it can be concluded that the administration of BC notably recovered the liver from hyperglycemia induced antioxidant imbalance, inflammation and apoptosis as well as rectified the imbalance in carbohydrate metabolizing enzymes.

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Curcumin and Quercetin Ameliorated Cypermethrin and Deltamethrin-Induced Reproductive System Impairment in Male Wistar Rats by Upregulating The Activity of Pituitary-Gonadal Hormones and Steroidogenic Enzymes.

Dietary antioxidants protect tissues and organs against insecticides/xenobiotic-induced damage. In the present study, we evaluated the results of exposure to synthetic pyrethroid insecticides, cypermethrin (Cyp) and deltamethrin (Del) and possible protective effects of curcumin and quercetin on reproductive system in male Wistar rats.

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Pharmacological Evaluation of Hepatoprotective Activity of AHPL/AYTAB/0613 Tablet in Carbon Tetrachloride-, Ethanol-, and Paracetamol-Induced Hepatotoxicity Models in Wistar Albino Rats.

Hepatotoxicity ultimately leads to liver failure. Conventional treatment options for hepatotoxicity are limited and not safe.

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Variation of genes involved in oxidative and nitrosative stresses in depression.

The dominating hypothesis among numerous hypotheses explaining the pathogenesis of depressive disorders (DD) is the one involving oxidative and nitrosative stress. In this study, we examined the association between single-nucleotide polymorphisms of the genes encoding SOD2 (superoxide dismutase 2), CAT (catalase), GPx4 (glutathione peroxidase 4), NOS1 (nitric oxide synthase 1), NOS2 (nitric oxide synthase 2), and the development of depressive disorders. Our study was carried out on the DNA isolated from peripheral blood collected from 281 depressed patients and 229 controls. Using TaqMan probes, we genotyped the following six polymorphisms: c.47T>C (p.Val16Ala) (rs4880) in SOD2, c.-89A>T (rs7943316) in CAT, c.660T>C (rs713041) in GPx4, c.-420-34221G>A (rs1879417) in NOS1, c.1823C>T (p.Ser608Leu) (rs2297518), and c.-227G>C (rs10459953) in NOS2. We found that the T/T genotype of the c.47T>C polymorphism was linked with an increased risk of depression. Moreover, the T/T genotype and T allele of c.660T>C increased the risk of DD occurrence, while the heterozygote and C allele decreased this risk. On the other hand, we discovered that the A/A genotype of c.-89A>T SNP was associated with a reduced risk of DD, while the A/T genotype increased this risk. We did not find any correlation between the genotypes/alleles of c.-420-34221G>A, c.1823C>T, and c.-227G>C, and the occurrence of DD. In addition, gene-gene and haplotype analyses revealed that combined genotypes and haplotypes were connected with the disease. Moreover, we found that sex influenced the impact of some SNPs on the risk of depression. Concluding, the studied polymorphisms of SOD2, CAT and GPx4 may modulate the risk of depression. These results support the hypothesis that oxidative and nitrosative stresses are involved in the pathogenesis of depressive disorders.

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Vitamin C attenuates biochemical and genotoxic damage in common carp (Cyprinus carpio) upon joint exposure to combined toxic doses of fipronil and buprofezin insecticides.

In the present study, potential protective role of Vitamin C (l-ascorbic acid) was investigated in aquaria acclimated common carp (Cyprinus carpio) following exposure for 96 h to combined toxic doses of fipronil (FP) and buprofezin (BPFN) insecticides in combination (FP: 200 μg/L; 4.57 × 10-7 mol/L and BPFN: 50 mg/L; 1.64 × 10-4 mol/L). At end of 96 h exposure, fish were supplemented with low (25 mg/L) and high (50 mg/L) doses of Vitamin C, added once daily to aquaria water for continuous three weeks. Appropriate control groups were run in parallel. Fish behavior was monitored throughout for signs of toxicity. At completion of experiments, liver, kidney, brain and gills were excised for toxicity assessment and possible remediation by the Vitamin C through biochemical determination of reactive oxygen species (ROS), thiobarbituric acid reactive substances or TBARS, reduced glutathione (GSH) and total protein content, levels of catalase (CAT), superoxide dismutase (SOD) and peroxidase (POD), and the Comet assay. Hepatosomatic index (HSI), condition factor (CF), survival rate (SR), and combination index (CI) were also determined. Data were compared statistically at p < 0.05. Results showed significant behavioral and biochemical alterations, and DNA damage in the fish group exposed to FP and BPFN in combination. In fish groups supplemented with Vitamin C following FP and BPFN treatment, significant alleviation in tissue damage and toxic effects was represented by substantial decreases in ROS and TBARS production (p < 0.001), along with a concomitant significant increase in the survival rate, GSH and total protein content, HSI, CF, and activities of SOD, CAT and POD enzymes (p < 0.001). Mean tail length of comet and percent tail DNA decreased significantly (p < 0.001), which indicated amelioration of DNA damage. The study concludes that Vitamin C is an effective remedial treatment against FP and BPFN-induced damage in exposed fish.

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