mRNA Expression Of Antioxidant Enzymes Research Articles

Interactive effect of boric acid and temperature stress on phenological characteristics and antioxidant system in Helianthus annuus L.

Plants have to cope with more than one abiotic stress at the same time in nature. Heat stress and mineral toxicity are at the forefront of these abiotic stresses. The purpose of this study is to investigate the interactive effects of high and low-temperature stress and boric acid application on the sunflower and reveal the potential protection mechanisms against the combined effect of two types of stress. Two different boric acid concentrations (10 and 25 mM) were applied to sunflowers grown separately at low (15 °C), optimum (25 °C) and high (40 °C) temperature. Then, root length and stem height, root and stem fresh-dry weight, root and stem biomass, malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and ascorbate peroxidase (APX) enzyme activities and changes in the gene expression levels of these enzymes were determined. It was determined that there were reductions in the phenological properties of the roots and stems of the samples grown at 40 °C based on the increasing boric acid concentration, while the samples grown at 15 °C were positively affected. The antioxidant enzyme activities and mRNA levels of the root and leaf samples at 40 °C were observed to increase. For the samples at 15 °C, the antioxidant enzyme activities and mRNA levels increased in the roots and decreased in the leaves. Considering phenological parameters, it was revealed that high boric acid application at low temperatures promoted plant growth, and considering the antioxidant enzyme activities and mRNA expression levels, it was highly effective in the plant's toleration of low temperatures.

Ameliorated effect of Lactobacillus plantarum SCS2 on the oxidative stress in HepG2 cells induced by AFB1

Aflatoxin B1 (AFB1), a widespread mycotoxin found in food, poses a significant threat to the food industry and production. The primary target of AFB1 is the liver. Probiotic-mediated antitoxicity has been proposed to overcome aflatoxin toxicity. In the present study, to investigate the protective effects and molecular mechanisms of Lactobacillus plantarum SCS2 (L. plantarum SCS2) against HepG2 cells oxidative stress induced by AFB1. HepG2 cells were cultured and treated with different concentrations of AFB1 (0-10 μmol/L) to induce oxidative stress and L. plantarum SCS2 (total protein, 0.4 mg/mL) was pretreated HepG2 for 2 h and then supplemented with AFB1 (10 μmol/L) for 22 h to observe cellular oxidative stress. The cytotoxicity, reactive oxygen species, malondialdehyde, activities and mRNA expressions of antioxidant enzymes and activation of the Nrf2 signaling pathway were measured. The results showed that AFB1 exposure caused oxidative stress in HepG2. Supplementation of L. plantarum SCS2 prevented AFB1-induced HepG2 cells activity decreased and activated antioxidant enzymes activity by inhibiting Nrf2 over expression. The results of in vitro experiments revealed that L. plantarum SCS2 evidently protected against AFB1-induced oxidative stress.

Nicotinamide mononucleotide supplementation protects the intestinal function in aging mice and D-galactose induced senescent cells.

The nicotinamide adenine dinucleotide (NAD+) level shows a temporal decrease during the aging process, which has been deemed as an aging hallmark. Nicotinamide mononucleotide (NMN), a key NAD+ precursor, shows the potential to retard the age-associated functional decline in organs. In the current study, to explore whether NMN has an impact on the intestine during the aging process, the effects of NMN supplementation on the intestinal morphology, microbiota, and NAD+ content, as well as its anti-inflammatory, anti-oxidative and barrier functions were investigated in aging mice and D-galactose (D-gal) induced senescent IPEC-J2 cells. The results showed that 4 months of NMN administration had little impact on the colonic microbiota and NAD+ content in aging mice, while it significantly increased the jejunal NAD+ content and improved the jejunal structure including increasing the villus length and shortening the crypt. Moreover, NMN supplementation significantly up-regulated the mRNA expression of SIRT3, SIRT6, nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), the catalytic subunit of glutamate-cysteine ligase (GCLC), superoxide dismutase 2 (SOD2), occludin, and claudin-1, but down-regulated the mRNA expression of tumor necrosis factor alpha (TNF-α). Specifically, in the D-gal induced senescent IPEC-J2 cells, 500 μM NMN restored the increased mRNA expression of interleukin 6 (IL6ST), IL-1A, nuclear factor (NF-κB1), and claudin-1 to normal levels to some extent. Furthermore, NMN treatment significantly affected the mRNA expression of antioxidant enzymes including NQO1, GCLC, SOD 2 and 3, and GSH-PX1, 3 and 4. In addition, 200 μM NMN enhanced the cell viability and total antioxidant capacity and lowered the reactive oxygen species level of senescent IPEC-J2 cells. Notably, NMN restored the down-regulated protein expression of occludin and claudin-1 induced by D-gal. The above data demonstrated the potential of NMN in ameliorating the structural and functional decline in the intestine during aging.

Protective effects of extracellular proteins of Saccharomycopsis fibuligera on UVA-damaged human skin fibroblasts

• We isolated and screened the Saccharomycopsis fibuligera strain SF-1 with high protein production from rice wine koji. • HPLC analysis showed that the molecular weight of SF-1-ECPs was less than 2000 Da, accounting for 22.28%. • The extracted SF-1-ECPs have strong antioxidant properties. • The antioxidant capacity of HSF and the enzymatic activity of MMP-1 were enhanced and weakened by SF-1-ECPs, respectively. • It was found that SF-1-ECPs improves the antioxidant capacity of HSF mainly by improving Nrf2/Keap1/Mafk signal transduction. Saccharomycopsis fibuligera is recognized as a food-based yeast which is widely used in food and drugs due to its high yield characteristics of extracellular enzymes. In this study, the extracellular proteins of S. fibuligera (SF-1-ECPs) are analyzed by HPLC, finding that 22.24% of the molecular weight of SF-1-ECPs is less than 2000 Da, and biochemical experiments, cell and cell molecular experiments are conducted to explore the significance of SF-1-ECPs in cosmetics. The results show that SF-1-ECPs can enhance antioxidant enzyme activity and mRNA expression within cells by using the Nrf2/Keap1/Mafk pathway to eliminate intracellular reactive oxygen, thereby protecting human skin fibroblasts from UVA-induced oxidative stress. They can also protect COL-I degradation caused by the increase of MMP-1 and thus delay skin aging.

Effect of starvation on the antioxidative pathway, autophagy, and mitochondrial function in the intestine of Chinese perch Siniperca chuatsi

The intestine is a main organ responsible for energy and nutrition absorption and digestion and is an important immune barrier in fish. In recent years, the intestinal health of fish has gained increasing attention in the aquaculture industry. The intestine is a direct target organ of starvation and is highly sensitive to nutritional changes. However, the adaptive responses of the fish intestine to starvation are not well studied. The present study aimed to reveal the effects of starvation on antioxidant systems, autophagy, and mitochondrial function in the intestine of Chinese perch. Therefore, Chinese perch (250 ± 22 g) were starved for 0, 7, and 14 days. Our results indicate that the contents of reactive oxygen species (ROS) and malondialdehyde (MDA) were significantly increased in the intestine of Chinese perch after 7 days and 14 days of starvation, indicating that starvation could induce oxidative stress in the intestine. Meanwhile, the activities and mRNA expression of antioxidative enzymes, including superoxide dismutases (SOD), glutathione peroxidases (GPx), and catalases (CAT), were upregulated in the intestine after the starvation treatment, which might be a compensatory response to oxidative stress. Starvation also increased the expression of nrf2 in the intestine, thereby resulting in the upregulation of antioxidative gene expression. However, the glutathione content and its generation in the intestine were decreased under starvation stress. The ultrastructural analysis of the intestine demonstrated that starvation induced autophagy in the intestine of Chinese perch. The RT–qPCR analysis showed that starvation induced the mRNA expression of genes involved in autophagosome membrane initiation, autophagosome membrane expansion, vesicle recycling, and cargo recruitment, including beclin1, ulk1, beclin1, lc3a, atg4, atg5, atg7, p62, and atg9. Mitochondria are the main ATP-generating organelles and target organelles for ROS. The present study indicates that starvation induced a decrease in the ATP content in the intestine of Chinese perch. In addition, starvation downregulated the expression of mitochondrial oxidative phosphorylation-related and mitochondrial ATP generation-related genes (cox1, atp5f1, atp5a1, and mt-cyb) in the intestine of Chinese perch, suggesting that starvation could suppress mitochondrial energy synthesis. Taken together, our data demonstrate that starvation can induce oxidative stress, disrupt antioxidant systems, and cause autophagy and mitochondrial dysfunction in the intestine of Chinese perch. These results provide insight into the mechanisms by which starvation disrupts intestinal homeostasis in fish.

The Protective Effect of Taurine on Oxidized Fish-Oil-Induced Liver Oxidative Stress and Intestinal Barrier-Function Impairment in Juvenile Ictalurus punctatus.

Dietary lipids provide energy for growth and development and provide fatty acids necessary for normal structure and biological function. However, oxidized lipids cause oxidative stress and intestinal damage. An 8-week feeding trial with fresh fish oil (FFO, control group), oxidized fish oil (OFO), and taurine-supplemented diets (OFOT, OFO + 0.2% of taurine) was conducted to evaluate the protective effect of taurine on oxidized fish-oil-induced liver oxidative stress and intestine impairment in juvenile Ictalurus punctatus. The results showed that (1) Growth performance was significantly lower in fish fed OFO than in those fed other diets, whereas the opposite occurred in the hepatosomatic index. (2) OFO-feeding significantly increased lipid deposition compared with the FFO group. The addition of taurine ameliorated the OFO-induced increase in lipid vacuolization in the liver, significantly upregulated lpl mRNA expression, and downregulated fas and srebp1 mRNA expression. (3) OFO-feeding significantly reduced oxidative damage of liver. Compared with the OFO group, the OFOT group remarkably upregulated antioxidant enzyme mRNA expression through the Nrf2-Keap1 signaling pathway based on the transcriptional expression. (4) OFO diets induced intestinal physical and immune barrier damage. Compared with the OFO group, OFOT diets remarkably downregulated il-1β, il-6, tnf-α, and il-8 mRNA expression and upregulated tgf-β mRNA expression through the NF-κB signaling pathway. Besides, the addition of taurine to OFO diets significantly upregulated zo-2 and zo-1 mRNA expression, and downregulated claudin-15 and claudin-12 mRNA expression. In conclusion, oxidized-fish-oil diets can cause negative physiological health effects in Ictalurus punctatus, while adding taurine can increase growth and antioxidant ability, reduce lipid deposition, and improve intestinal health.

Protective Effect of Natural Antioxidant Compounds on Methimazole Induced Oxidative Stress in a Feline Kidney Epithelial Cell Line (CRFK).

The treatment of choice for feline hyperthyroidism is the administration of the antithyroid drug methimazole. Both the endocrinopathy and the drug adverse reactions (e.g., hepatotoxicosis, gastrointestinal disorders, and renal injury) are partly due to oxidative stress and redox unbalance. This study investigated the free radical production and the impairment of the antioxidant barrier induced by methimazole in an in vitro model of feline renal epithelium. The protective effects of quercetin and resveratrol were also explored. CRFK cells were incubated with a methimazole concentration equivalent to the maximum plasma levels in orally treated cats (4 µM), in the presence or absence of either one of the two selected antioxidants at different time-points (up to 72 h). Cell viability, ROS production, GSH levels, and mRNA expression of antioxidant enzymes (i.e., CAT, SOD, GPx, and GST) were assessed. Methimazole impaired cell viability and increased ROS levels in a time-dependent manner. Similarly, GSH content and CAT, SOD, and GPx3 expression were higher compared with control cells. Such effects were significantly counteracted by quercetin. These results provide new insights about the mechanisms underlying the methimazole-related side effects frequently observed in hyperthyroid cats. They also support the use of quercetin in the management of feline hyperthyroidism.

The alleviative effects of taurine supplementation on growth, antioxidant enzyme activities, hepatopancreas morphology and mRNA expression of heat shock proteins in freshwater prawn Macrobrachium nipponense (De Haan) exposed to dietary lead stress

To investigate the potential alleviative effect of taurine supplementation on growth and oxidant stress in freshwater prawn Macrobrachium nipponense (De Haan) exposed to dietary lead, pelleted feeds were prepared with two concentrations of lead (0 and 10 mg/kg diet) and two levels of taurine (0 and 15 g/kg diet). Healthy prawns were randomly distributed between the four treatment groups, with three tanks per group and 50 prawns per tank. Dietary lead decreased weight gain and the activities of superoxide dismutase, catalase and glutathione peroxidase; increased malondialdehyde content; altered hepatopancreas morphology; and decreased the expression of heat shock protein 90 (HSP90; p < .05). A significant interactive effect was found between dietary lead and taurine on the malondialdehyde level, and taurine supplementation significantly decreased the malondialdehyde level under lead stress (p < .05). No significant effect on growth, hepatopancreas morphology and HSP90 expression was observed with taurine supplementation under lead stress. Overall, dietary lead affected growth, induced oxidative stress and impaired hepatopancreas morphology of the prawns, and dietary taurine significantly alleviated oxidative stress through a decreased malondialdehyde level, whereas the capacity of taurine to alleviate the decreased growth rate, hepatopancreas damage and low HSP90 expression under lead stress was limited.

Protein hydrolysates from Pleurotus geesteranus obtained by simulated gastrointestinal digestion exhibit neuroprotective effects in H2 O2 -injured PC12 cells.

Neurodegenerative diseases are considered to be among the diseases most threatening to human beings. Increasing evidence shows that antioxidant hydrolysates/peptides with neuroprotective effects may relieve neurodegenerative diseases. However, related research in mushrooms, one of the richest sources of antioxidant hydrolysates/peptides, is in its infancy. Therefore, the in vitro neuroprotective effects of protein hydrolysates from Pleurotus geesteranus were researched in this study. Proteins were extracted from P. geesteranus and then hydrolyzed by simulated gastrointestinal digestion. The neuroprotective effects of the protein hydrolysates were evaluated by H2 O2 -injured PC12 cells. The hydrolysates showed a superior antioxidative ability and had a higher abundance of hydrophobic amino acids (e.g., leucine, alanine, and phenylalanine). Neither cytotoxicity nor the increase of ROS in PC12 cells was observed under treatment with the hydrolysates. However, pre-treatment with the hydrolysates in PC12 cells, which were then injured by H2 O2 , markedly attenuated ROS generation and enhanced the activities and mRNA expression of the endogenous antioxidant enzymes (catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD)), leading to a 26.68% increase in cell viability. The hydrolysates exhibited strong neuroprotective activity in H2 O2 -injured PC12 cells, possibly by reducing ROS generation and enhancing the activity of the antioxidant enzymatic system. PRACTICAL APPLICATIONS: Antioxidant hydrolysates with neuroprotection were obtained from Pleurotus geesteranus proteins by simulating gastrointestinal digestion, which exhibited an excellent pre-protective effect in oxidatively damaged PC12 cells. Further study showed that hydrolysates pre-protection may exert antioxidant activities not only as an exogenous antioxidant to scavenge ROS but also as a gene regulator to modulate the endogenous antioxidant enzymes gene expression. These results indicated that the potential of antioxidant peptides, derived from P. geesteranus through gastrointestinal digestion, could serve as a source of bioactive molecules in the prevention, relief or even treatment of neurodegenerative disorders.

Aloe vera increases mRNA expression of antioxidant enzymes in cryopreserved bovine ovarian tissue and promotes follicular growth and survival after in vitro culture

The aims of the present study were to evaluate the effects of Aloe vera extract on expression of mRNA for antioxidant enzymes in bovine ovarian tissue after vitrification, as well as on follicular morphology, viability, activation and extracellular matrix in cultured ovarian tissues that had been previously vitrified. Fragments from bovine ovarian cortical tissue were cryopreserved in a vitrification solution alone or supplemented with two concentrations of Aloe vera (10 or 50%). After thawing, the cryopreserved tissues were analyzed by histological techniques, as well as the levels of mRNA for SOD, CAT, PRDX6 and GPX1 were investigated. Furthermore, cryopreserved fragments were then culture in vitro in α-MEM for 6 days. Histological evaluation of cultured tissues was performed to determine the percentages of normal and developing follicles. The results showed that, after vitrification, the presence of Aloe vera in both concentrations was able to maintain percentages of collagen fibers similar to fresh tissues (P < 0.05). Aloe vera in both concentrations significantly increased mRNA levels for PRDX6 and GPX1 in cryopreserved tissues, while 10% Aloe vera increased mRNA levels for SOD (P < 0.05). In parallel, after in vitro culture, fragments vitrified in the presence of 10% Aloe vera had significantly higher levels of morphologically healthy follicles when compared to tissue that were vitrified without Aloe vera. In fragments vitrified with Aloe vera, the rate of developing follicles was significantly higher than in tissues vitrified without Aloe vera. Tissues vitrified with 10% Aloe vera and cultured in vitro maintained percentages of collagen fibers similar to fresh tissues. In conclusion, 10% Aloe vera increases the expression of mRNA for PRDX6, GPX1 and SOD in vitrified ovarian tissues, maintains follicular survival and promotes activation and development of follicles after in vitro culture of vitrified bovine ovarian tissue.

Dietary resveratrol attenuation of intestinal inflammation and oxidative damage is linked to the alteration of gut microbiota and butyrate in piglets challenged with deoxynivalenol

BackgroundDeoxynivalenol (DON) is a widespread mycotoxin that induces intestinal inflammation and oxidative stress in humans and animals. Resveratrol (RES) effectively exerts anti-inflammatory and antioxidant effects. However, the protective effects of RES on alleviating DON toxicity in piglets and the underlying mechanism remain unclear. Therefore, this study aimed to investigate the effect of RES on growth performance, gut health and the gut microbiota in DON-challenged piglets. A total of 64 weaned piglets [Duroc × (Landrace × Yorkshire), 21-d-old, 6.97 ± 0.10 kg body weight (BW)] were randomly allocated to 4 treatment groups (8 replicate pens per treatment, each pen containing 2 males; n = 16 per treatment) for 28 d. The piglets were fed a control diet (CON) or the CON diet supplemented with 300 mg RES/kg diet (RES group), 3.8 mg DON/kg diet (DON) or both (DON+RES) in a 2 × 2 factorial design.ResultsDON-challenged piglets fed the RES-supplemented diet had significantly decreased D-lactate concentrations and tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β) mRNA and protein expression, and increased zonula occludens-1 (ZO-1) mRNA and protein expression compared with those of DON-challenged piglets fed the unsupplemented diet (P < 0.05). Compared with unsupplemented DON-challenged piglets, infected piglets fed a diet with RES showed significantly decreased malondialdehyde (MDA) levelsand increased mRNA expression of antioxidant enzymes and antioxidant genes (i.e., GCLC, GCLM, HO-1, SOD1 and NQO-1) and glutamate-cysteine-ligase modulatory subunit (GCLM) protein expression (P < 0.05). Moreover, RES supplementation significantly abrogated the increase in the proportion of TUNEL-positive cells and the protein expression of caspase3 in DON-challenged piglets (P < 0.05). Finally, RES supplementation significantly increased the abundance of Roseburia and butyrate concentrations, while decreasing the abundances of Bacteroides and unidentified-Enterobacteriaceae in DON-challenged piglets compared with DON-challenged piglets alone (P < 0.05).ConclusionsRES supplementation improved gut health in DON-challenged piglets by strengthening intestinal barrier function, alleviating intestinal inflammation and oxidative damage, and positively modulating the gut microbiota. The protective effects of RES on gut health may be linked to increased Roseburia and butyrate concentrations, and decreased levels of Bacteroides and unidentified-Enterobacteriaceae.

Effects of Supplementation with Dried Neem Leaf Extract on Lipid Peroxidation and Antioxidant Enzyme mRNA Expression in the Pectoralis Major Muscle of Broiler Chickens.

This study was conducted to evaluate the effects of dietary supplementation of dried neem (Azadirachta indica) leaf extract (DNE) on lipid peroxidation and the expression of genes encoding mRNAs in antioxidant enzymes in the pectoralis major muscle of chickens. A total of 24 male broiler chickens (ROSS308) were divided into three groups (n=8) at 21 days of age. The control group of chickens was fed a basal diet, and the remaining two groups of chickens were fed a basal diet supplemented with DNE at a concentration of 0.5% or 2.0% until 35 days of age. Growth performance (body weight, weight gain, feed intake, and feed conversion ratio) and tissue weights did not differ among the three groups. The 2.0% DNE-supplemented diet decreased the muscle malondialdehyde content, a marker of lipid peroxidation, and drip loss compared to the control chickens. In addition, the expression of genes encoding mRNAs of antioxidant enzymes (i.e., Cu/Zn-superoxide dismutase, Mn-superoxide dismutase, glutathione peroxidase 7, and catalase) were higher in the pectoralis major muscle of chickens fed the 2.0% DNE-supplemented diet than in the control chickens. Therefore, DNE supplementation increased the expression of genes encoding mRNAs in antioxidant enzymes and reduced lipid peroxidation and drip loss in the pectoralis major muscle of broiler chickens.

Molecular mechanisms of zooplanktonic toxicity in the okadaic acid-producing dinoflagellate Prorocentrum lima.

Prorocentrum lima is a dinoflagellate that forms hazardous blooms and produces okadaic acid (OA), leading to adverse environmental consequences associated with the declines of zooplankton populations. However, little is known about the toxic effects and molecular mechanisms of P.lima or OA on zooplankton. Here, their toxic effects were investigated using the brine shrimp Artemia salina. Acute exposure of A.salina to P.lima resulted in lethality at concentrations 100-fold lower than densities observed during blooms. The first comprehensive results from global transcriptomic and metabolomic analyses in A.salina showed up-regulated mRNA expression of antioxidant enzymes and reduced non-enzyme antioxidants, indicating general detoxification responses to oxidative stress after exposure to P.lima. The significantly up-regulated mRNA expression of proteasome, spliceosome, and ribosome, as well as the increased fatty acid oxidation and oxidative phosphorylation suggested the proteolysis of damaged proteins and induction of energy expenditure. Exposure to OA increased catabolism of chitin, which may further disrupt the molting and reproduction activities of A.salina. Our data shed new insights on the molecular responses and toxicity mechanisms of A.salina to P.lima or OA. The simple zooplankton model integrated with omic methods provides a sensitive assessment approach for studying hazardous algae.

Dexmedetomidine attenuates H2O2-induced apoptosis of rat cardiomyocytes independently of antioxidant enzyme expression

Introduction and ObjectivesDexmedetomidine is a highly selective alpha-2 adrenoceptor agonist that has sedative and analgesic properties and myocardial protective effects. However, the mechanism underlying the protective effect of dexmedetomidine on cardiomyocytes remains unknown. This study mainly aimed to investigate the effects of dexmedetomidine on the generation of reactive oxygen species (ROS) in cardiomyocytes and whether it inhibits the apoptosis of cardiomyocytes by affecting antioxidant enzyme expression. MethodsNeonatal rat cardiomyocytes were pretreated with dexmedetomidine (100 nM) for 24 h. The cardiomyocytes were then incubated with 200 μM hydrogen peroxide solution (H2O2) for 4 h. PCR assay was used to determine the mRNA expression of antioxidant enzymes. Western blot assay was used to determine the protein expression of antioxidant enzymes. Fluorescence microscopy with the MitoSOX probe was used to detect the formation of ROS in cardiomyocytes, and fluorescence-activated cell sorting with annexin V/PI was used to determine the number of apoptotic cardiomyocytes. ResultsDexmedetomidine reduced ROS generation and antioxidant enzymes levels in cardiomyocytes before H2O2 stimulation (p<0.05). However, ROS generation and apoptosis in cardiomyocytes were significantly increased after H2O2 treatment, and dexmedetomidine pretreatment markedly inhibited the changes (p<0.05). ConclusionFor the first time, to the best of our knowledge, our study shows that dexmedetomidine has a protective effect on cardiomyocytes through inhibition of ROS-induced apoptosis, and more importantly, this effect is independent of antioxidant enzyme mRNA and protein expression.

Dietary exposure to methyl mercury chloride induces alterations in hematology, biochemical parameters, and mRNA expression of antioxidant enzymes and metallothionein in Nile tilapia.

Methyl mercury chloride "MMC" (CH3ClHg) is an ubiquitous environmental toxicant that causes a variety of adverse effects. In the present study, we investigated the effects of sub-chronic toxicity of MMC on Nile tilapia (Oreochromis niloticus) through the evaluation of growth performance and hematological, biochemical, and oxidative stress biomarkers. From 150 healthy fish, five equally sized treatment groups were created: a control (CT) group fed with a basal diet and four MMC treatment groups exposed to 0.5, 1, 1.5, and 2 mg of MMC per kg of basal diet for 60 days. MMC exposure significantly reduced the growth performance and survival of O. niloticus and decreased red blood cell count and hemoglobin concentration. Treated fish exhibited normocytic normochromic anemia in addition to leucopenia, lymphopenia, granulocytopenia, and monocytopenia. Moreover, MMC exposure significantly affected liver function, including a reduction in the total protein levels while increasing cholesterol and triglyceride levels. It also markedly increased the production of stress biomarkers such as glucose and cortisol levels. Furthermore, MMC significantly elevated the levels of hepatic enzymes, induced tissue damage, and caused inflammation, as indicated by the upregulation of mRNA expression of hepatic metallothionein. Finally, MMC exposure induced oxidative stress by altering the antioxidant status of the liver and downregulating the mRNA expression of superoxide dismutase, glutathione peroxidase, and glutathione S-reductase. In conclusion, MMC toxicity induced hematological and biochemical alterations, leading to an enhanced state of oxidative stress in O. niloticus.

Zinc loaded whey protein nanoparticles mitigate the oxidative stress and modulate antioxidative gene expression in testicular tissues in rats

This study aimed to utilize whey protein nanoparticles (WPNPs) and zinc (Zn) loaded WPNPs to protect against carbon tetrachloride (CCl4)-induced testicular damage in rats. Zn was loaded on WPNPs at three levels and Zn release was determined at different time intervals. Seventy male Wistar rats were divided into 7 groups and treated orally for 4 weeks as follows: the control group, CCl4-treated group (0.5 ml/100 g b.w) twice a week, CCl4 plus WPNPs-treated group (300 mg/kg b.w), CCl4 plus Zn citrate-treated group (50 mg/kg b.w), and the groups treated with CCl4 plus the three Zn-WPNPs formulations. Blood and testicular tissue samples were collected for different assays. Animals treated with CCl4 showed a significant decrease in body weight and relative weight of the testis, testosterone level, antioxidant enzymes activity and mRNA expression of Nrf2, HO-1 and NQO1 and increased Malondialdehyde (MDA), nitric oxide (NO) and mRNA expression of Keep1 and induced histological changes in the testis. WPNPs alone, Zn alone or Zn loaded WPNPs at the three levels protect against CCl4-induced testicular damage. These effects were more pronounced in the group received the fabrication with low Zn level. This study concluded that Zn-WPNPs could reduce the oxidative stress in the testicular tissue via different mechanisms mainly via the regulation of Nrf2-Keap1 antioxidative signaling pathway.

Effects of ammonia-N stress on the antioxidant enzymes, heat shock proteins, and apoptosis-related genes of Macrobrachium rosenbergii

Current study explored the acute toxicity and oxidative stress of ammonia-N on Macrobrachium rosenbergii. Prawns were exposed to ammonia-N at 3.01, 3.55, 4.18, 4.92, 5.80, 6.82, and 8.04 mg·L−1 for a 96 h acute toxicity test. In the subsequent sublethal toxicity text, they were exposed to ammonia-N at 0.5 or 1.88 mg·L−1 (1/2 96 h LC50) for 3, 8, 12, 24, 48, and 72 h. The total superoxide dismutase (T-SOD) activity, catalase (CAT) activity and malondialdehyde (MDA) content were detected in the muscle, haemolymph, and gill. The gene expression of antioxidases (Cu/ZnSOD, CAT, GPX), heat shock proteins (HSP60, HSP70, HSP90), and apoptosis-related genes (Caspase 3, Bok) in the muscle and hepatopancreas also was evaluated. The LC50 values of non-ionic ammonia at 24, 48, 72, and 96 h were 7.72, 5.44, 4.28, and 3.78 mg·L−1, respectively. Ammonia-N significantly affected the T-SOD and CAT activities in the haemolymph and gill but not in the muscle. After 72 h of ammonia-N exposure, MDA content in the muscle, haemolymph, and gill in 1.88 mg·L−1 group significantly increased. The relative mRNA expression of antioxidant enzymes, heat shock proteins and Caspase 3 were upregulated in the hepatopancreas and muscle after ammonia exposure, especially in 1.88 mg·L−1. This result suggested that 1/2 96 h LC50 ammonia exposure induced severe oxidative stress, eventually even apoptosis of M. rosenbergii through the caspase pathway. Highlights Half of 96 h LC50 ammonia-N caused severe oxidative stress on M. rosenbergii. Ammonia-N induced the antioxidase and HSP to protect cells from oxidative stress. Ammonia-N induced mRNA expression level of Caspase 3 of M. rosenbergii.

Maternal high-fructose consumption provokes placental oxidative stress resulting in asymmetrical fetal growth restriction in rats.

We aimed to determine the impact of high-fructose intake during pregnancy on the fetal-placental unit in rats, which may be the initial mechanism of the programming effect of fructose. Pregnant Sprague–Dawley rats were randomly assigned to three groups and respectively provided tap water (n = 10), 10% (w/v) fructose solution (n = 10), and 10% (w/v) glucose solution (n = 10) from embryonic day 0 to 20. Compared with the control and glucose groups, significantly lower fetal length, fetal weight, placental weight, and fetus/placenta ratio were found in the fructose group on embryonic day 20 (all p<0.05). In parallel with markedly increased uric acid concentrations in the dams, significantly decreased antioxidant enzymes activities and mRNA expression levels were observed in placentas in the fructose group (all p<0.05). In the fructose group, placental mRNA and protein expression of nuclear factor erythroid 2-related factor 2 was markedly downregulated and kelch-like ECH-associated protein 1 was significantly upregulated (all p<0.05). In conclusion, high-fructose consumption during pregnancy drives augmented oxidative stress in rats. Placental insufficiency under oxidative stress contributes to asymmetrical fetal growth restriction.

Oral consumption of α-glucosyl-hesperidin could prevent lens hardening, which causes presbyopia

Presbyopia is one of the most well-known diseases of the eye, predominantly affecting the adult population after 50 years’. Due to hardening of the lens and failure of accommodative change, patients lose the ability to focus on near objects. This eye symptom is reported to be an early symptom of age-related nuclear cataract, and we have previously reported that hesperetin treatment could delay the onset of nuclear cataractogenesis induced by sodium selenite. In this study, we examined whether oral intake of α-glucosyl-hesperidin (G-Hsd), which has greater water solubility than hesperetin, could delay the onset of presbyopia. G-Hsd treatment protected lens elasticity, upregulated the mRNA expression of anti-oxidative enzymes like glutathione reductase and thioredoxin reductase 1 in the plasma and lens, and prevented premature cataract symptoms in selenite-induced cataract rat lens. Thus, the anti-presbyopic effects of G-Hsd were attributed, at least in part, to its antioxidant effects. G-Hsd represents the first oral treatment agent with anti-presbyopia and/or anti-cataract properties.

Morinda officinalis polysaccharides improve meat quality by reducing oxidative damage in chickens suffering from tibial dyschondroplasia

Tibial dyschondroplasia (TD) is the common leg disease in commercial broilers. However, the effects of TD on meat quality and the protective of Morinda officinalis polysaccharide (MOP) are largely unknown. Three hundred broiler chicks (one-day-old) were equally allocated into control (CON), TD and MOP-treated groups for 15 days. The results indicated that TD influenced morphology and meat quality-related parameters of the breast muscle, and changed the activity and mRNA expression of antioxidant enzymes in plasma and breast muscles. Moreover, metabolomics profiling of breast muscle revealed that the main altered metabolites 4-guanidinobutyric acid and chenodeoxycholic acid, which are related to meat quality and oxidative stress. Additionally, 500 mg/L MOP effectively restored the content of meat metabolites and oxidative damage. These findings suggest that oxidative damage caused by TD may affect meat quality in broilers by changing the content of breast muscle metabolites and that MOP supplementation has a restorative effect.