Effects of Nostoc commune extract on the cerebral oxidative and neuroinflammatory status in a mice model of schizophrenia.

Cyanobacterium Nostoc commune has long been used to alleviate various diseases. This research examines the effects of Nostoc commune extract (NCE) against behavioral disorders, cerebral oxidative stress, and inflammatory damage in the ketamine-induced schizophrenia model. Oral NCE administration (70 and 150 mg/kg/d) is performed after intraperitoneal ketamine injection (20 mg/kg) for 14 consecutive days. The forced swimming and open field tests are used to assess schizophrenia-like behaviors. After the behavioral test, dopamine (DA) level, oxidative stress markers, as well as the interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) expression are measured in the cerebral cortex. The results show that NCE treatment ameliorates KET-induced anxiety and depressive-like behaviors in OFT and FST, respectively. NCE considerably decreases the malondialdehyde (MDA) and DA levels and IL-6 and TNF-α expressions in mice with schizophrenia-like symptoms. Also, a significant increase is observed in the glutathione (GSH) level and catalase (CAT), superoxide dismutase (SOD), and glutathione reductase (GRx) activity in cerebral tissue. The present study shows that NCE treatment effectively improves KET-induced schizophrenia-like behaviors and oxidative and inflammatory damage. Therefore, NCE, via its bioactive constituents, could have strong neuroprotective effects in the schizophrenia-like model.

Stress responses to warming in Japanese flounder (Paralichthys olivaceus) from different environmental scenarios.

Japanese flounder (Paralichthys olivaceus) is one of cold-water species widely farmed in Asia. In recent years, the increased frequency of extreme weather events caused by global warming has led to serious impact on Japanese flounder. Therefore, it is crucial to understand the effects of representative coastal economic fish under increasing water temperature. In this study, we investigated the histological and apoptosis responses, oxidative stress and transcriptomic profile in the liver of Japanese flounder exposed to gradual temperature rise (GTR) and abrupt temperature rise (ATR). The histological results showed liver cells in ATR group were the most serious in all three groups including vacuolar degeneration and inflammatory infiltration, and had more apoptosis cells than GTR group detected by TUNEL staining. These further indicated ATR stress caused more severe damage than GTR stress. Compared with control group, the biochemical analysis showed significantly changes in two kinds of heat stress, including GPT, GOT and D-Glc in serum, ATPase, Glycogen, TG, TC, ROS, SOD and CAT in liver. In addition, the RNA-Seq was used to analyze the response mechanism in Japanese flounder liver after heat stress. A total of 313 and 644 differentially expressed genes (DEGs) were identified in GTR and ATR groups, respectively. Further pathway enrichment of these DEGs revealed that heat stress affected cell cycle, protein processing and transportation, DNA replication and other biological processes. Notably, protein processing pathway in the endoplasmic reticulum (ER) was enriched significantly in KEGG and GSEA enrichment analysis, and the expression of ATF4 and JNK was significantly up-regulated in both GTR and ATR groups, while CHOP and TRAF2 were high expressed in GTR and ATR groups, respectively. In conclusion, heat stress could cause tissue damage, inflammation, oxidative stress and ER stress in the liver of Japanese flounder. The present study would provide insight into the reference for the adaptive mechanisms of economic fish in face of increasing water temperature caused by global warming.

Intestinal Damages by F18+Escherichia coli and Its Amelioration with an Antibacterial Bacitracin Fed to Nursery Pigs.

This study investigated intestinal oxidative damage caused by F18+Escherichia coli and its amelioration with antibacterial bacitracin fed to nursery pigs. Thirty-six weaned pigs (6.31 ± 0.08 kg BW) were allotted in a randomized complete block design. Treatments were: NC, not challenged/not treated; PC, challenged (F18+E. coli at 5.2 × 109 CFU)/not treated; AGP challenged (F18+E. coli at 5.2 × 109 CFU)/treated with bacitracin (30 g/t). Overall, PC reduced (p < 0.05) average daily gain (ADG), gain to feed ratio (G:F), villus height, and villus height to crypt depth ratio (VH:CD), whereas AGP increased (p < 0.05) ADG, and G:F. PC increased (p < 0.05) fecal score, F18+E. coli in feces, and protein carbonyl in jejunal mucosa. AGP reduced (p < 0.05) fecal score and F18+E. coli in jejunal mucosa. PC reduced (p < 0.05) Prevotella stercorea populations in jejunal mucosa, whereas AGP increased (p < 0.05) Phascolarctobacterium succinatutens and reduced (p < 0.05) Mitsuokella jalaludinii populations in feces. Collectively, F18+E. coli challenge increased fecal score and disrupted the microbiota composition, harming intestinal health by increasing oxidative stress, and damaging the intestinal epithelium, ultimately impairing growth performance. Dietary bacitracin reduced reduced F18+E. coli populations and the oxidative damages they cause, thereby improving intestinal health and the growth performance of nursery pigs.

Solid and modified biochars mitigate root cell lignification and improve nutrients uptake in mint plants under fluoride and cadmium stresses.

Lignification is a physiological process that reduces pollutants' entrance into plant root cells via blocking apoplastic pathways. The closure of apoplastic pathways can also decrease the nutrients' uptake by roots. Application of biochar as an efficient soil amendment might be useful in increasing nutrients influx into root cells by decreasing lignification. Therefore, this experiment was performed to examine the conceivable effects of biochar forms [solid and chemically altered biochars with H2O2, KOH and H3PO4 (25 g biochar forms kg-1 soil)] on modifying lignification process and nutrients uptake by mint (Mentha crispa L.) plants under toxicity of cadmium and fluoride. The biochar treatments boosted plant root growth and activity as well as the real content and maximum sorption capacity of Zn, Fe, Mg, and Ca under stressful conditions. In contrast, biochar treatments increased root cell viability and reduced fluoride and cadmium contents, and oxidative damages under stressful conditions. The biochar treatments decreased the activity of phenylalanine ammonia-lyase and peroxidase enzymes under toxic conditions, which led to a decrease in the contents of lignin and its monomers (p-hydroxybenzaldehyde, guaiacyl, and syringaldehyde) in the roots. Solid biochar was less effective than engineered biochars in reducing root cell lignification. Therefore, addition of biochar forms to the soil could be an effective way to reduce root cell lignification and enhance nutrients uptake by plants under cadmium and fluoride toxicities.

Entomotherapeutic Role of Periplaneta americana Extract in Alleviating Aluminum Oxide Nanoparticles-Induced Testicular Oxidative Impairment in Migratory Locusts (Locusta migratoria) as an Ecotoxicological Model.

In this study, we shed light for the first time on the usage of migratory locusts (Locusta migratoria) as an insect model to investigate the nanotoxicological influence of aluminum oxide (Al2O3) nanoparticles at low doses on testes, and evaluate the capacity of a whole-body extract of American cockroaches (Periplaneta americana) (PAE) to attenuate Al2O3 NPs-induced toxicity. Energy dispersive X-ray microanalyzer (EDX) analysis verified the bioaccumulation of Al in testicular tissues due to its liberation from Al2O3 NPs, implying their penetration into the blood-testis barrier. Remarkably, toxicity with Al engendered disorders of antioxidant and stress biomarkers associated with substantial DNA damage and cell apoptosis. Furthermore, histopathological and ultrastructural analyses manifested significant aberrations in the testicular tissues from the group exposed to Al2O3 NPs, indicating the overproduction of reactive oxygen species (ROS). Molecular docking analysis emphasized the antioxidant capacity of some compounds derived from PAE. Thus, pretreatment with PAE counteracted the detrimental effects of Al in the testes, revealing antioxidant properties and thwarting DNA impairment and cell apoptosis. Moreover, histological and ultrastructural examinations revealed no anomalies in the testes. Overall, these findings substantiate the potential applications of PAE in preventing the testicular impairment of L. migratoria and the conceivable utilization of locusts for nanotoxicology studies.

Endogenous production of ω-3 polyunsaturated fatty acids mitigates cisplatin-induced myelosuppression by regulating NRF2-MDM2-p53 signaling pathway.

Cisplatin is a chemotherapy medication used to treat a wide range of cancers. A common side effect of cisplatin is myelosuppression. Research suggests that oxidative damages are strongly and consistently related to myelosuppression during cisplatin treatment. ω-3 polyunsaturated fatty acids (PUFAs) can enhance the antioxidant capacity of cells. Herein, we investigated the protective benefit of endogenous ω-3 PUFAs on cisplatin-induced myelosuppression and the underlying signaling pathways using a transgenic mfat-1 mouse model. The expression of mfat-1 gene can increase endogenous levels of ω-3 PUFAs by enzymatically converting ω-6 PUFAs. Cisplatin treatment reduced peripheral blood cells and bone marrow nucleated cells, induced DNA damage, increased the production of reactive oxygen species, and activated p53-mediated apoptosis in bone marrow (BM) cells of wild-type mice. In the transgenics, the elevated tissue ω-3 PUFAs rendered a robust preventative effect on these cisplatin-induced damages. Importantly, we identified that the activation of NRF2 by ω-3 PUFAs could trigger an antioxidant response and inhibit p53-mediated apoptosis by increasing the expression of MDM2 in BM cells. Thus, endogenous ω-3 PUFAs enrichment can strongly prevent cisplatin-induced myelosuppression by inhibiting oxidative damage and regulating the NRF2-MDM2-p53 signaling pathway. Elevation of tissue ω-3 PUFAs may represent a promising treatment strategy to prevent the side effects of cisplatin.

Insight into the Mechanism of Salt-Induced Oxidative Stress Tolerance in Soybean by the Application of Bacillus subtilis: Coordinated Actions of Osmoregulation, Ion Homeostasis, Antioxidant Defense, and Methylglyoxal Detoxification.

Considering the growth-promoting potential and other regulatory roles of bacteria, we investigated the possible mechanism of the role of Bacillus subtilis in conferring salt tolerance in soybean. Soybean (Glycine max cv. BARI Soybean-5) seeds were inoculated with B. subtilis, either through a presoaking with seeds or a direct application with pot soil. After 20 days of sowing, both the seed- and soil-inoculated plants were exposed to 50, 100, and 150 mM of NaCl for 30 days. A clear sign of oxidative stress was evident through a remarkable increase in lipid peroxidation, hydrogen peroxide, methylglyoxal, and electrolyte leakage in the salt treated plants. Moreover, the efficiency of the ascorbate (AsA)-glutathione (GSH) pathways was declined. Consequently, the plant growth, biomass accumulation, water relations, and content of the photosynthetic pigments were decreased. Salt stress also caused an increased Na+/K+ ratio and decreased Ca2+. On the contrary, the B. subtilis inoculated plants showed increased levels of AsA and GSH, their redox balance, and the activities of the AsA-GSH pathway enzymes, superoxide dismutase, catalase, glutathione peroxidase, glutathione S-transferase, and peroxidase. The B. subtilis inoculated plants also enhanced the activities of glyoxalase enzymes, which mitigated methylglyoxal toxicity in coordination with ROS homeostasis. Besides this, the accumulation of K+ and Ca2+ was increased to maintain the ion homeostasis in the B. subtilis inoculated plants under salinity. Furthermore, the plant water status was uplifted in the salt treated soybean plants with B. subtilis inoculation. This investigation reveals the potential of B. subtilis in mitigating salt-induced oxidative stress in soybean plants through modulating the antioxidant defense and glyoxalase systems along with maintaining ion homeostasis and osmotic adjustments. In addition, it was evident that the soil inoculation performed better than the seed inoculation in mitigating salt-induced oxidative damages in soybean.

Brassinosteroid Supplementation Alleviates Chromium Toxicity in Soybean (Glycine max L.) via Reducing Its Translocation.

Chromium (Cr) phytotoxicity severely inhibits plant growth and development which makes it a prerequisite to developing techniques that prevent Cr accumulation in food chains. However, little is explored related to the protective role of brassinosteroids (BRs) against Cr-induced stress in soybean plants. Herein, the morpho-physiological, biochemical, and molecular responses of soybean cultivars with/without foliar application of BRs under Cr toxicity were intensely investigated. Our outcomes deliberated that BRs application noticeably reduced Cr-induced phytotoxicity by lowering Cr uptake (37.7/43.63%), accumulation (63.92/81.73%), and translocation (26.23/38.14%) in XD-18/HD-19, plant tissues, respectively; besides, improved seed germination ratio, photosynthetic attributes, plant growth, and biomass, as well as prevented nutrient uptake inhibition under Cr stress, especially in HD-19 cultivar. Furthermore, BRs stimulated antioxidative defense systems, both enzymatic and non-enzymatic, the compartmentalization of ion chelation, diminished extra production of reactive oxygen species (ROS), and electrolyte leakage in response to Cr-induced toxicity, specifically in HD-19. In addition, BRs improved Cr stress tolerance in soybean seedlings by regulating the expression of stress-related genes involved in Cr accumulation, and translocation. Inclusively, by considering the above-mentioned biomarkers, foliar spray of BRs might be considered an effective inhibitor of Cr-induced damages in soybean cultivars, even in Cr polluted soil.

Apigenin alleviates cancer drug Sorafenib induced multiple toxic effects in Swiss albino mice via anti-oxidative stress.

Sorafenib is an FDA-approved chemotherapeutic drug used as standard therapy for advanced-stage cancers. However, Sorafenib-induced multiple adverse effects are a major limitation that directly impacts patients' physical and physiological well-being. Therefore, it is vital to identify agents that can lessen the associated adverse effects and enhance efficacy. Apigenin, a dietary plant flavone, is a bioactive-compound present in fruits and vegetables having anti-oxidant, anti-inflammatory, and anti-cancer properties. Our study aimed to investigate Sorafenib-induced toxic effects at genomic, cellular, and tissue level and the potential protective effects of Apigenin. To achieve our goal, we treated Swiss albino mice with Apigenin (50 mg/kg bw) alone or in combination with Sorafenib (40 mg/kg bw). Next, we performed DNA interaction, genotoxicity, oxidative damages, anti-oxidant activities, liver enzyme levels, and histopathological studies. We demonstrated that Apigenin and Sorafenib bind DNA via electrostatic interaction. Further, Sorafenib induces genetic, oxidative, and tissue damages characterized by an increase in chromosomal aberrations and micronucleus, reactive oxygen species (ROS) and reactive nitrogen species (RNS), oxidative and DNA damage, lipid peroxidation, and hepato-renal damages, and a decrease in antioxidant-enzymes. Interestingly, the Sorafenib-induced adverse effects were ameliorated by Apigenin. Our findings indicate that Apigenin has protective effects against Sorafenib-induced toxicity and could be combined with Sorafenib to lessen its adverse effects and enhance its efficacy. However, further pre-clinical and clinical studies are required to evaluate Apigenin's effectiveness with Sorafenib.

Influence and Implications of the Molecular Paradigm of Nitric Oxide Underlying Inflammatory Reactions of the Gastrointestinal Tract of Dog: A Major Hallmark of Inflammatory Bowel Disease.

Nitric oxide (NO), a pleiotropic free radical messenger molecule, is responsible for the various cellular function of the gastrointestinal mucosa. It plays a major role in the maintenance of perfusion, regulation of microvascular, epithelial permeability, and immune functions. Nitric oxide exerts its beneficial effect on the initiation and maintenance of inflammation in human inflammatory bowel disease (IBD). But the accelerated production of NO triggers activation of the inducible form of the NO synthase enzyme (iNOS) that leads to damages of the intestinal membrane. Nitric oxide synthase enzyme is responsible for the higher production of NO from l-arginine and causes an inflammatory condition in the intestinal epithelium. Nitric oxide induces nitrative DNA damage and oxidative DNA damage in the cellular system. Accelerated production of NO enhances iNOS activity that is associated with cytotoxicity and apoptosis of gastrointestinal epithelial cells in the dog. Chronic inflammation leads to angiogenesis that is modulated by the immune system in IBD. Chronic inflammation is a major risk factor for the development of gastrointestinal malignancies. Nitric oxide participates in mucosal inflammation in the intestine through invigoration of NO synthase enzyme. The intrinsic complex mechanism is correlated with the inflammation in the gastrointestinal tract and is also correlated with the expression of iNOS, enzymatic activity and NO production. Nitric oxide employs a significant role in modulating epithelial permeability with accelerated immune response in acute colitis. But the enormous generation of NO causes adverse effects on the mucosal cell during the inflammatory process in IBD. In this review, a complex episode of NO generation with altered biochemical pathways was assessed for the regulation of mucosal inflammation in inflammatory bowel disease of dogs. This review is a unique compilation of the role of NO in the pathogenesis of inflammatory bowel disease of dogs. Nitric oxide plays a key role in modulating cancer in the gastrointestinal tract. This review seeks to explore the characteristics of NO as a major hallmark of canine inflammatory bowel diseases.

Inflammatory bowel disease (IBD), the most significant chronic inflammatory condition, is characterized by the painful infection in the gastrointestinal tract among dogs. Nitric oxide (NO) plays a significant role in counteracting the inflammation in the mucosa of the intestine. But prolonged chronic inflammation in the submucosal layers leads to accelerated production of NO that causes harmful effects on the cellular system of the intestine of IBD cases. In IBD, a complex mechanism has occurred in the intestine of dogs.

Alpha Lipoic Acid as a Protective Mediator for Regulating the Defensive Responses of Wheat Plants against Sodic Alkaline Stress: Physiological, Biochemical and Molecular Aspects.

Recently, exogenous α-Lipoic acid (ALA) has been suggested to improve the tolerance of plants to a wide array of abiotic stresses. However, there is currently no definitive data on the role of ALA in wheat plants exposed to sodic alkaline stress. Therefore, this study was designed to evaluate the effects of foliar application by ALA at 0 (distilled water as control) and 20 µM on wheat seedlings grown under sodic alkaline stress (50 mM 1:1 NaHCO3 & Na2CO3; pH 9.7. Under sodic alkaline stress, exogenous ALA significantly (p ≤ 0.05) improved growth (shoot fresh and dry weight), chlorophyll (Chl) a, b and Chl a + b, while Chl a/b ratio was not affected. Moreover, leaf relative water content (RWC), total soluble sugars, carotenoids, total soluble phenols, ascorbic acid, K and Ca were significantly increased in the ALA-treated plants compared to the ALA-untreated plants. This improvement was concomitant with reducing the rate of lipid peroxidation (malondialdehyde, MDA) and H2O2. Superoxide dismutase (SOD) and ascorbate peroxidase (APX) demonstrated greater activity in the ALA-treated plants compared to the non-treated ones. Conversely, proline, catalase (CAT), guaiacol peroxidase (G-POX), Na and Na/K ratio were significantly decreased in the ALA-treated plants. Under sodic alkaline stress, the relative expression of photosystem II (D2 protein; PsbD) was significantly up-regulated in the ALA treatment (67% increase over the ALA-untreated plants); while Δ pyrroline-5-carboxylate synthase (P5CS), plasma membrane Na+/H+ antiporter protein of salt overly sensitive gene (SOS1) and tonoplast-localized Na+/H+ antiporter protein (NHX1) were down-regulated by 21, 37 and 53%, respectively, lower than the ALA-untreated plants. These results reveal that ALA may be involved in several possible mechanisms of alkalinity tolerance in wheat plants.

Protective Effect of Nanoselenium on Renal Oxidative Damage Induced by Mercury in Laying Hens.

This study investigated the effects of dietary nanoselenium (nano-Se) supplementation protecting from renal oxidative damages induced by mercury (Hg) exposure in laying hens. Furthermore, endoplasmic reticulum (ER) stress pathway was explored to reveal the protective mechanism of nano-Se. A total of 576 40-week-old Hyline-White laying hens were randomly allocated to 4 groups with 6 pens per group and 24 hens per pen. The experimental groups were as follows: control (basal diet), control + 27.0 mg/kg Hg, control + 5.0 mg/kg nano-Se, and Hg27.0 + 5.0 mg/kg nano-Se. The results revealed that dietary Hg exposure significantly reduced laying performance (P < 0.05) and egg quality (P < 0.05), whereas nano-Se supplementation partially reversed the reductions. Besides, dietary Hg exposure could induce histopathology damages and apoptosis in kidney, whereas nano-Se addition could alleviate these toxicities effectively. After Hg exposure, the activities and gene expressions of superoxidative dismutase (SOD) (P < 0.05), catalase (CAT) (P < 0.01), glutathione reductase (GR) (P < 0.05) and glutathione peroxidase (GSH-Px) (P < 0.05), and glutathione (GSH) content (P < 0.05) were significantly decreased, while the malondialdehyde (MDA) level was significantly increased (P < 0.05) in kidney. However, nano-Se supplementation partially reversed the levels and gene expressions of these antioxidant biomarkers in kidney. Furthermore, dietary Hg exposure significantly increased the gene expressions of PERK (P < 0.05), ATF4 (P < 0.05), CHOP (P < 0.05), IRE1α (P < 0.05), TRAF2 (P < 0.05), ASK1 (P < 0.05), Caspase-9 (P < 0.05), Caspase-8 (P < 0.05), Caspase-3 (P < 0.05), and Bax/Bcl-2 (P < 0.05), whereas nano-Se supplementation partially reversed these increases of gene expressions. In summary, this study provides evidence that dietary Hg exposure can induce renal oxidative damages, and elucidates an important role of ER stress pathway in nano-Se alleviating renal apoptosis in laying hens.

Accumulation of Carbonyl Proteins in the Brain of Mouse Model for Methylglyoxal Detoxification Deficits.

Recent studies have shown that carbonyl stress is a causative factor of schizophrenia, categorized as carbonyl stress-related schizophrenia (CS-SCZ). However, the correlation between carbonyl stress and the pathogenesis of this disease is not well established. In this study, glyoxalase 1(Glo1)-knockout and vitamin B6-deficient mice (KO/VB6 (-) mice), which are susceptible to methylglyoxal (MGO)-induced oxidative damages, were used as a CS-SCZ model to analyze MGO-modified protein and the carbonyl stress status in the brain. A comparison between Wild/VB6(+) mice and KO/VB6(-) mice for accumulated carbonyl proteins levels, with several advanced glycation end products (AGEs) in the brain, revealed that carbonyl protein levels with the Nδ-(5-hydro-5-methyl-4-imidazolon-2-yl) ornithine (MG-H1) moiety were significantly increased in the hippocampus, prefrontal cortex, striatum, cerebral cortex, and brainstem regions of the brain in KO/VB6(-) mice. Moreover, two-dimensional electrophoresis and Liquid chromatography-tandem mass spectrometry analysis showed MG-H1-modified arginine residues in mitochondrial creatine kinase, beta-adrenergic receptor kinase 1, and T-complex protein in the hippocampus region of KO/VB6(-) mice, but not in Wild/VB6(+) mice. In particular, MG-H1 modification of mitochondrial creatine kinase was quite notable. These results suggest that further studies focusing on MG-H1-modified and accumulated proteins in the hippocampus may reveal the onset mechanism of CS-SCZ induced by MGO-induced oxidative damages.

Potential Protective Role of Cyrtopodion Scabrum in Antioxidant Parameters in Serum and Liver of Rats with 5-FU-Induced Oxidative Damage.

Chemotherapy is the main approach for the treatment of cancer; however, it often causes unpleasant oxidative damages. Therefore, the development of an effective alternative/complementary therapy with improved tumor suppression efficiency and lower adverse effects is highly required. Recently, it has been shown that Cyrtopodion scabrum extract (CsE) is an effective and selective tumor suppressor medicine. The present study investigated the antioxidant activity of Cyrtopodion scabrum homogenate (CsH) and CsE and their effects on attenuating 5-fluorouracil (5-FU)-induced liver dysfunction in rats. A total of 60 male rats (weight: 200-220 g) were divided into six groups and treated for 14 days. The control (group I) and 5-FU (group II) groups received distilled water and 5-FU, respectively. The other four groups were orally administered with CsE, CsH, CsE+5-FU, and CsH+5-FU (groups III to VI), respectively by gavages based on a daily schedule. The 5-FU-induced oxidative damage was evaluated by changes in the weight and food and water intake during the treatment and antioxidant parameters in the liver and serum of the treated rats. The obtained data indicated that the administration of CsH and CsE significantly improved liver function and defense system of antioxidants by attenuating the levels or activities of malondialdehyde, superoxide anion, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase and decrease of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione S-transferase, total antioxidant capacity, glutathione, total protein, and albumin in the liver and serum, induced by 5-FU treatment. The obtained data of the current study suggested that CsH and CsE play a protective role in the imbalance elicited by 5-FU and can be used as alternative/complementary supplements with 5-FU to reduce oxidative damages which is the consequence of reactive oxygen species production in cancerous patients.

The Feasibility of Antioxidants Avoiding Oxidative Damages from Reactive Oxygen Species in Cryopreservation.

Cryopreservation prolongs the storage time of cells and plays an important role in modern biology, agriculture, plant science and medicine. During cryopreservation, cells may suffer many damages, such as osmotic dehydration, large ice puncture and oxidative damages from reactive oxygen species (ROS). Classic cryoprotectants (CPAs) are failing to dispose of ROS, while antioxidants can turn ROS into harmless materials and regulate oxidative stress. The combination of antioxidants and CPAs can improve the efficiency of cryopreservation while negative results may occur by misuse of antioxidants. This paper discussed the feasibility of antioxidants in cryopreservation.

Gallic acid improves the antioxidant ability against cadmium toxicity: Impact on leaf lipid composition of sunflower (Helianthus annuus) seedlings.

In the present work, the effect of seed pre-soaking with gallic acid (GA; 3,4,5-triphydroxyl-benzoic acid) in conferring subsequent tolerance to Cd stress in sunflower (Helianthus annuus) seedlings was investigated. Exposing sunflower seedlings to increasing Cd concentrations (5, 10 and 20 µM) caused a gradual decrease in root and shoot biomass and increased the metal accumulation in both organs. Seed pretreatment with 75 µM GA significantly restricted Cd uptake, markedly alleviated Cd-induced plant growth inhibition, and mitigated the oxidative damages caused by this metal, as compared to plants directly exposed to Cd. GA pre-soaking prior to Cd stress also enhanced catalase, ascorbate peroxidase and glutathione reductase activities, while inhibiting that of superoxide dismutase. This was associated with increased levels of total thiols and glutathione along with a decreased level of oxidized glutathione in leaves. Moreover, GA pre-soaking led to changes in leaf fatty acid composition of seedlings challenged with Cd, as evidenced by the higher total lipid content and lipid unsaturation degree. As a whole, this study provides strong arguments highlighting the potential role of GA as a growth promoter for sunflower seedlings submitted to Cd stress, notably by boosting the antioxidant defense system and improving leaf membrane stability.

Jasmonic acid-mediated enhanced regulation of oxidative, glyoxalase defense system and reduced chromium uptake contributes to alleviation of chromium (VI) toxicity in choysum (Brassica parachinensis L.).

The cultivation of leafy vegetables on metal contaminated soil embodies a serious threat to yield and quality. In the present study, the potential role of exogenous jasmonic acid (JA; 0, 5, 10, and 20 µM) on mitigating chromium toxicity (Cr; 0, 150, and 300 µM) was investigated in choysum (Brassica parachinensis L.). With exposure to increasing Cr stress levels, a dose-dependent decline in growth, photosynthesis, and physio-biochemical attributes of choysum plants was observed. An increase in Cr levels also resulted in oxidative stress closely associated with higher lipoxygenase activity (LOX), hydrogen peroxide (H2O2) generation, lipid peroxidation (MDA), and methylglyoxal (MG) levels. Exogenous application of JA alleviated the Cr-induced phytotoxic effects on photosynthetic pigments, gas exchange parameters, and restored growth of choysum plants. While exposed to Cr stress, JA supplementation induced plant defense system via enhanced regulation of antioxidant enzymes, ascorbate and glutathione pool, and the glyoxalase system enzymes. The coordinated regulation of antioxidant and glyoxalase systems expressively suppressed the oxidative and carbonyl stress at both Cr stress levels. More importantly, JA restored the mineral nutrient contents, restricted Cr uptake, and accumulation in roots and shoots of choysum plants when compared to the only Cr-stressed plants. Overall, the application of JA2 treatment (10 µM JA) was more effective and counteracted the detrimental effects of 150 µM Cr stress by restoring the growth and physio-biochemical attributes to the level of control plants, while partially mitigated the detrimental effects of 300 µM Cr stress. Hence, JA application might be considered as an effective approach for minimizing Cr uptake and its detrimental effects in choysum plants grown on contaminated soils.

Secondary metabolites of Galactomyces geotrichum from Laminaria japonica ameliorate cognitive deficits and brain oxidative stress in D-galactose induced Alzheimer's disease mouse model.

Accumulating evidences have shown the beneficial effects of natural products for Alzheimer's disease (AD) treatment. The present study was designed to investigate the neuroprotective effects of secondary metabolites of Galactomyces geotrichum (SMGG) on D-galactose induced AD mice. SMGG was extracted and its toxicological evaluation was conducted. To explore the neuroprotective mechanism responsible for anti-AD activity of SMGG, spatial learning and memory behavioral, oxidative stress levels, acetylcholinesterase and choline acetyltransferase activity assays were employed. The AD mice received SMGG treatment exhibited significant improvement in cognitive performance, enhanced antioxidant capacity, decreased acetylcholinesterase activity and increased choline acetyltransferase activity. Meanwhile, SMGG had no toxicity and seven compounds were separated from it: 7,8-dimethyl-iso-alloxazine, 1-methyl-3-benzyl-6-(4-hydroxybenzyl)-2,5-piperzainedione, cyclo-(Phe-Pro), cyclo-(Leu-Pro), cyclo-(Pro-Gly), cyclo-(Gly-Leu) and uracil, respectively. Overall, these data suggested that SMGG protects the brain against D-galactose induced cognitive impairment, oxidative damages and acetylcholine content decrease in AD mice.

Differential lead-fluoride and nickel-fluoride uptake in co-polluted soil variably affects the overall physiome in an aromatic rice cultivar.

The present study aimed to show that nickel and fluoride exhibited synchronized co-inhibited uptake in the aromatic rice cultivar, Gobindobhog, since bioaccumulation of the two elements was lower than that during individual stress, so that overall growth under combined stress was similar to control seedlings. On the contrary, lead and fluoride stimulated their co-uptake which triggered oxidative damages, NADPH oxidase activity, methylglyoxal accumulation, photosynthetic inhibition, membrane-protein damages, necrosis and genomic template degradation. Accumulation of proline, anthocyanins, non-protein thiols and phytochelatins was stimulated for systemic protection against reactive oxygen species (ROS) and xenobiotic-mediated injuries during lead-fluoride toxicity. ROS accumulation during nickel-fluoride stress was insignificant due to which enhanced accumulation of most antioxidants was not required. Glutathione depletion during combined lead-fluoride toxicity was due to its utilization in the glyoxalase cycle and also inhibition of glutathione reductase. However, the nickel-fluoride-treated sets maintained glutathione reserves and glyoxalase activity similar to those in control. Presence of fluoride 'safeguarded' the glutathione-utilizing enzymes like glutathione reductase, glutathione peroxidase and glutathione-S-transferase during dual lead-fluoride stress. This was because these enzymes showed higher activity compared to that under lead toxicity alone. Enzymatic antioxidants like superoxide dismutase, ascorbate peroxidase and guaiacol peroxidase were activated during lead-fluoride toxicity due to altered iron and copper homeostasis. Catalase activity was strongly inhibited, resulting in the inability to scavenge H2O2 and suppression of the fluoride-adaptable phenotype. However, none of the enzymatic antioxidants were inhibited during nickel-fluoride stress, which cumulatively allowed the seedlings to maintain normal physiology. Overall our findings holistically reveal the physiological plasticity of Gobindobhog in response to two different heavy metals under the influence of fluoride.

Copper Toxicity Links to Pathogenesis of Alzheimer's Disease and Therapeutics Approaches.

Alzheimer's disease (AD) is an irreversible, age-related progressive neurological disorder, and the most common type of dementia in aged people. Neuropathological lesions of AD are neurofibrillary tangles (NFTs), and senile plaques comprise the accumulated amyloid-beta (Aß), loaded with metal ions including Cu, Fe, or Zn. Some reports have identified metal dyshomeostasis as a neurotoxic factor of AD, among which Cu ions seem to be a central cationic metal in the formation of plaque and soluble oligomers, and have an essential role in the AD pathology. Cu-Aß complex catalyzes the generation of reactive oxygen species (ROS) and results in oxidative damage. Several studies have indicated that oxidative stress plays a crucial role in the pathogenesis of AD. The connection of copper levels in AD is still ambiguous, as some researches indicate a Cu deficiency, while others show its higher content in AD, and therefore there is a need to increase and decrease its levels in animal models, respectively, to study which one is the cause. For more than twenty years, many in vitro studies have been devoted to identifying metals' roles in Aß accumulation, oxidative damage, and neurotoxicity. Towards the end, a short review of the modern therapeutic approach in chelation therapy, with the main focus on Cu ions, is discussed. Despite the lack of strong proofs of clinical advantage so far, the conjecture that using a therapeutic metal chelator is an effective strategy for AD remains popular. However, some recent reports of genetic-regulating copper transporters in AD models have shed light on treating this refractory disease. This review aims to succinctly present a better understanding of Cu ions' current status in several AD features, and some conflicting reports are present herein.