Levels Of Antioxidant Enzymes Research Articles

Modulation of the crosstalk between Keap1/Nrf2/HO-1 and NF-κB signaling pathways by Tomatidine protects against inflammation/oxidative stress-driven fulminant hepatic failure in mice

Fulminant hepatic failure (FHF) is the terminal phase of acute liver injury, which is characterized by massive hepatocyte necrosis and rapid hepatic dysfunction in patients without preexisting liver disease. There are currently no therapeutic options for such a life-threatening hepatic failure except liver transplantation; therefore, the terminal phase of the underlying acute liver injury should be avoided. Tomatidine (TOM), asteroidal alkaloid, may have different biological activities, including antioxidant and anti-inflammatory effects. Herein, the lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced FHF mouse model was established to explore the protective potential of TOM and the underlying mechanisms of action. TOM pretreatment significantly inhibited hepatocyte necrosis and decreased serum aminotransferase activities in LPS/D-GalN-stimulated mice. TOM further increased the level of different antioxidant enzymes while reducing lipid peroxidation biomarkers in the liver. These beneficial effects of TOM were shown to be associated with targeting of NF-κB signaling pathways, where TOM repressed NF-κB activation and decreased LPS/D-GalN-induced TNF-α, IL-6, IL-1β, and iNOS production. Moreover, TOM prevented LPS/D-GalN-induced upregulation of Keap1 expression and downregulation of Nrf2 and HO-1 expression, leading to increased Nrf2-binding activity and HO-1 levels. Besides, TOM pretreatment repressed LPS/D-GalN-induced upregulation of proliferating cell nuclear antigen (PCNA) expression, which spared the hepatocytes from damage and subsequent repair following the LPS/D-GalN challenge. Collectively, our findings revealed that TOM has a protective effect on LPS/D-GalN-induced FHF in mice, showing powerful antioxidant and anti-inflammatory effects, primarily mediated via modulating Keap1/Nrf2/HO-1 and NF-κB/TNF-α/IL-6/IL-1β/iNOS signaling pathways.

Beneficial Effects of Probiotics on Liver Injury Caused by Chronic Alcohol Consumption

Alcoholic liver injury is a serious risk to human health. Probiotics have become a popular form of treatment. Lacticaseibacillus casei Grx12 and Limosilactobacillus fermentum Grx07 isolated from the gut of long-lived people in Rugao, Jiangsu, were studied to determine their protective effects and possible mechanisms of action on alcoholic liver injury. The results showed that rat serum ALT and AST were restored, and liver injury was reduced after the probiotics intervention. The level of antioxidant enzymes and antioxidants such as SOD, GSH and GSH-Px in the rat liver was significantly increased (p < 0.05), which reduces the level of MDA, a peroxidation product in the liver, and thus alleviates liver oxidative stress. L. casei Grx12 and L. fermentum Grx07 also could significantly enhance the expression of Nrf2 protein in the rat liver to regulate the anti-oxidative stress response in the body and cells (p < 0.05). The levels of ADH, Na+-K+-ATPase and Ca2+-ATPase in the rat liver were significantly increased (p < 0.05), which enhanced the body’s metabolism of alcohol. The rat serum LPS and liver TNF-α, IL-6, VEGF, TGF-β1 and NF-κB levels were significantly reduced (p < 0.05), indicating that the probiotics could relieve liver inflammation. The results of this study indicate that L. casei Grx12 and L. fermentum Grx07 have certain protective effects on alcoholic liver injury in rats, likely because of their antioxidant properties and ability to prevent oxidative stress and relieve inflammation.

Cyto and Genoprotective Potential of Tannic Acid Against Cadmium and Nickel Co-exposure Induced Hepato-Renal Toxicity in BALB/c Mice.

Tannic acid (TA) is a metal chelating polyphenol that plays a crucial role in metal detoxification, but its modulatory role in co-exposure of these heavy metals' exposure needs to be explored. Cadmium (Cd) and nickel (Ni) are inorganic hazardous chemicals in the environment. Humans are prone to be exposed to the co-exposure of Cd and Ni, but the toxicological interactions of these metals are poorly defined. Present study was undertaken to study the preventive role of TA in Cd-Ni co-exposure-evoked hepato-renal toxicity in BALB/c mice. In the current investigation, increased oxidative stress in metal intoxicated groups was confirmed by elevated peroxidation of the lipids and significant lowering of endogenous antioxidant enzymes. Altered hepato-renal serum markers, DNA fragmentation, and histological alterations were also detected in the metal-treated groups. Present study revealed that Cd is a stronger toxicant than Ni and when co-exposure was administered, additive, sub-additive, and detrimental effects were observed. Prophylactic treatment with TA significantly reinstated the levels of lipid peroxidation (LPO), non-enzymatic, and enzymatic antioxidants. Moreover, it also restored the serum biomarker levels, DNA damage, and histoarchitecture of the given tissues. TA due to its metal chelating and anti-oxidative properties exhibited cyto- and genoprotective potential against Cd-Ni co-exposure-induced hepatic and renal injury.

A Comprehensive Review on Therapeutic Properties of Camel Milk

Background: Camel milk has been traditionally valued for its nutritional and medicinal properties across various cultures. Recent scientific inquiries have illuminated its potential in treating a range of health conditions, including diabetes, autism, allergies, liver and kidney functions, and infectious diseases such as tuberculosis. This has sparked a growing interest in integrating camel milk into health and dietary regimens as a natural therapeutic agent. Objective: The objective of this review is to systematically examine the therapeutic properties of camel milk, focusing on its application in treating specific diseases, its nutritional composition, and its implications for human healthcare. Methods: This review synthesized data from various studies that investigated the medicinal benefits of camel milk in treating diseases like diabetes, hepatitis C, autism, allergies, and tuberculosis. The methods involved a comprehensive literature search across several databases, including PubMed, Scopus, and Google Scholar, to collect studies that reported on the therapeutic effects, nutritional composition, and health outcomes associated with camel milk consumption. Results: Findings indicate that camel milk contains unique molecules such as insulin-like proteins, amylase, lactoferrin, and specific enzymes beneficial for managing diabetes, hepatitis C, and allergies. Studies on autistic children showed improvements in antioxidant enzyme levels after camel milk consumption. In tuberculosis patients, camel milk consumption was associated with improved clinical symptoms and increased immunoglobulin levels. The nutritional analysis revealed camel milk's rich composition in essential fats, proteins, lactose, and minerals, highlighting its nutritional value. Conclusion: Camel milk presents a viable, natural therapeutic option for a variety of health conditions, offering significant benefits in nutritional and medicinal applications. Its integration into dietary practices and healthcare could enhance human health outcomes, particularly in areas where conventional medical resources are scarce or in populations seeking alternative treatments.

Therapeutic potential of Bhiramiyadhi bhavanai choornam in ameliorating scopolamine-induced impaired learning and memory in rats: neuroprotective effects and mechanistic insights

This study intended to explore Bhiramiyadhi bhavanai choornam’s (BBC) effect on scopolamine-induced impaired learning and memory in rats. BBC was prepared and subjected to organoleptic and phytochemical investigations. Scopolamine (2mg/kg, i.p.) was injected into all animals except for the vehicle control group. Donepezil 1mg/kg and BBC (215, 430, and 860mg/kg along with a 1:1 ratio of ghee and honey) were administered orally for 14 days to respective groups. The effect of BBC on locomotor activity, olfactory and spatial memory and exploratory behaviour was evaluated. Later, animals were sacrificed, and brain homogenates were tested for levels of malondialdehyde, antioxidant enzymes, acetylcholinesterase, nitric oxide and TNF-α. A statistical evaluation was carried out. Investigating BBC for phytoconstituents, showed that steroids, phenols, tannins, quinones, alkaloids, flavonoids, glycosides, terpenoids and carbohydrates were present. Treatment with BBC reversed scopolamine-induced learning and memory impairment by significantly (p < 0.001) improving behaviour in the Y maze, novel object recognition test and MWM. BBC also decreased oxidative stress induced by scopolamine by increasing reduced levels of antioxidant enzymes and declining MDA, AChE, NO, and TNF- α levels in the rat brain in a rat model of scopolamine-induced learning and memory impairment.

Effect of salinity on the toxicokinetics, oxidative stress, and metallothionein gene expression in Meretrix meretrix exposed to cadmium

To understand the effect of salinity on the toxicokinetics, oxidative stress, and detoxification of cadmium-exposed Meretrix meretrix, M. meretrix were acclimatized to different salinities (8, 14, 20, 26, and 32 ppt) for 14 d, exposed to 10 μg/L Cd for 7 d, followed by a 28-day depuration period. The internal Cd concentration was determined, and the activities of antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), and glutathione-S-transferase (GST)), and the malondialdehyde (MDA) content were measured. The mRNA expression levels of antioxidant enzyme (Cu/Zn SOD, CAT) and detoxification-related genes metallothionein (MT) were analyzed. The mean concentrations of Cd in M. meretrix tissues were in the order gill > digestive gland > mantle > axe foot. The Cd uptake rate in the four tissues decreased with increasing salinity (range: 14–26 ppt). The Cd elimination half-lives were the highest at 8 ppt and 14 ppt salinity. Cadmium activated the four oxidative stress-related related enzymes in the gills. At the end of accumulation period, Cd exposure at 20 ppt salinity significantly increased the expression of Cu/Zn SOD. CAT expression was significantly inhibited at 20 ppt salinity, but was induced at 32 ppt. MT mRNA expression was only induced under Cd at 20 ppt salinity. At the end of depuration period, Cu/Zn SOD expression was inhibited at salinities of 8, 14, and 26 ppt. The results indicated that SOD, CAT, GST, MDA, Cu/Zn SOD, CAT, and MT were sensitive to cadmium in a water environment, and can be used as indicators of marine heavy metal pollution.

Anticancer Action of Silver Nanoparticles in SKBR3 Breast Cancer Cells through Promotion of Oxidative Stress and Apoptosis.

Silver nanoparticles (AgNPs) are known as one of the highly utilized NPs owing to their unique characteristics in the field of cancer research. The goal of this research was to explore the oxidative stress, apoptosis, and angiogenesis in SKBR3 breast cancer cells after exposure to AgNPs. The survival rate of SKBR3 cancer cells and MCF-10A normal breast cells was assessed under the effects of different concentrations (0, 32, 64, 128, and 250 μg/ml) by MTT method. The oxidative condition was assessed by measuring reactive oxygen species (ROS) production, total oxidant status (TOS), total antioxidant capacity (TAC), malondialdehyde (MDA), and antioxidant enzyme activity (CAT, GPx, and CAT) using colorimetric-based kits. Flow cytometry and Hoechst 33258 staining were performed to investigate the induction of apoptosis. Furthermore, the expression of Bcl-2-associated X protein (Bax), B-cell lymphoma 2 (Bcl-2), and caspase 3 and 7 activity was measured. The cell migration and vascular endothelial growth factor-A (VEGF-A) gene expression, protein kinase B (AKT), phosphatidylinositol 3-kinase (PI3K) were also studied. The MTT results indicated that AgNPs inhibit the SKBR3 cells' viability in a concentration-dependent way. Besides, AgNPs markedly induced oxidative stress via increasing TOS content, MDA production, reduction of TAC, and regulation of antioxidant enzyme level. Additionally, AgNPs promoted apoptosis as revealed by an enhancement in Bax/Bcl-2 expression ratio. Findings also indicated that AgNPs suppress the expression of genes (VEGF-A, AKT, and PI3K) involved in angiogenesis. Altogether, our data revealed that AgNPs initiate oxidative stress and apoptosis in SKBR3 breast cancer cells, dose dependently.

Pulmonary toxicity associated with high-dose favipiravir and treatment options: biochemical and histopathological evaluation.

Favipiravir is a broad-spectrum antiviral drug that is a viral RNA-dependent RNA polymerase inhibitor. Favipiravir is used in high doses to treat COVID-19 but has a side effect on humans at high doses. The side effects of favipiravir have been associated with oxidative stress in the literature. In this trial, we investigated the biochemical and histopathological effects of lacidip-ine, thiamine pyrophosphate (TTP), and adenosine triphosphate (ATP), drugs with antioxidant properties, on the lung toxicity caused by high-dose favipiravir in rats. The rats were classified into five groups: healthy (HG), favipiravir alone (Fav), lacidipine+favipiravir (LFav), TPP+favipiravir (TFav), and ATP+favipiravir (AFav). Favipiravir (800 mg/kg) was administered twice daily for seven days. Laci-dipine (4 mg/kg), TPP (20 mg/kg), and ATP (25 mg/kg) were administered once daily for seven days. Oxidant (malondialdehyde), non-enzymatic (total glutathi-one), and enzymatic (superoxide dismutase and catalase) antioxidant levels were measured in the excised lung tissues. Furthermore, the tissues were histopatho-logically examined. The systemic administration of high doses of favipiravir in-creased oxidant levels and decreased antioxidant levels in the lung tissue of rats. In parallel, the histopathological examination of the lung tissue revealed the presence of severe mononuclear cell infiltrations in interstitial areas and pronounced lymphoid hyperplasia. Lacidipine exhibited superior efficacy in mit-igating oxidative stress and preventing the decline of antioxidants induced by favipiravir compared with TPP and ATP. Histopathologically, the lacidipine admin-istration significantly reduced lung oxidative damage. TTP moderately reduced severe favipiravir-associated lung injury. However, ATP was ineffective against fa-vipiravir-associated lung injury. Lacidipine offers more therapeutic benefits than TPP in treating oxidative lung injury caused by high doses of favipiravir.

Anti-fatigue effect of Lateolabrax japonicus peptides in mice and the underlying action mechanism via in vitro and in vivo assays

Fatigue is a common health issue in today's society worldwide. Finding anti-fatigue functional substances seems warranted to alleviate fatigue-related issues. The Lateolabrax japonicus peptides (LPH) obtained via enzymatic hydrolysis were identified being rich in Glu, Gly, and hydrophobic amino acids, which exhibited antioxidant properties. However, other biological functions of LPH have yet to be reported. This study main goal was to investigate the anti-fatigue effects of LPH via a fatigue mice model, and further to elucidate its underlying mechanism using in vivo assay. The results indicated that LPH exhibited strong antioxidant activity and stability in vitro. Meanwhile, LPH significantly extended the swimming time of mice, while also decreasing fatigue marker levels (LA, BUN, CK, and MDA) in serum concurrently by increased levels of antioxidant enzymes, blood glucose, and Na+-K+-ATPase. Histopathological examination revealed that LPH effectively improved tissue damage caused by fatigue. Mechanistically, LPH upregulated the gene and protein expression of Nrf2 and AMPK, indicating its regulatory role in Keap1/Nrf2 and AMPK/SIRT1/PGC-1α/NRF1 signaling pathways. Furthermore, the study demonstrated that LPH could modulate the abundance and balance of fatigue-related gut microbiota (Butyricimonas, Helicobacter, Monoglobus, and Turicibacter). In summary, these findings indicated that LPH exerted its anti-fatigue effect by improving energy metabolism and reducing oxidative stress, suggesting its potential as a promising functional anti-fatigue nutraceutical in food industry.

Metagenomic and biochemical analyses reveal the potential of silicon to alleviate arsenic toxicity in rice (Oryza sativa L.)

Arsenic (As) pollution in agricultural systems poses a serious threat to crop productivity and food safety. Silicon (Si) has been reported to mitigate toxic effects of heavy metals in plants. However, the mechanisms behind Si-mediated alleviation of As toxicity in rice (Oryza sativa L.) remain poorly understood. Here, we performed metagenomic and biochemical analyses to investigate the potential of Si in alleviating As toxicity to rice plants. As exposure reduced plant growth, chlorophyll contents, antioxidant enzyme levels and soil enzymes activity, while increasing reactive oxygen species (ROS) activity and inducing alterations in the rhizosphere microbiome of rice seedlings. Silicon amendments enhanced rice growth (24%), chlorophyll a (25%), and chlorophyll b (26.7%), indicating enhanced photosynthetic capacity. Si amendments also led to the upregulation of antioxidant enzymes viz., superoxide dismutase (15.4%), and peroxidase (15.6%), resulting in reduced ROS activity and oxidative stress compared to the As-treated control. Furthermore, Si treatment reduced uptake and translocation of As in rice plants, as evidenced by the analysis of elemental contents. Microscopic examination of leaf and root ultrastructure showed that Si mitigated As-induced cellular damage and maintained normal morphology. Metagenomic analysis of the rice rhizosphere microbiome revealed that Si application modulated composition and diversity of microbial communities e.g., Proteobacteria, Actinobacteria, and Firmicutes. Additionally, Si amendments upregulated the relative expression levels of OsGSH, OsPCs, OsNIP1;1 and OsNIP3;3 genes, while the expression levels of the OsLis1 and OsLis2 genes were significantly downregulated compared with As-treated rice plants. Overall, these findings contribute to our understanding of Si-mediated plant resilience to As stress and offer potential strategies for sustainable agriculture in As-contaminated regions.

Oxidative stress in metabolic dysfunction-associated steatotic liver disease (MASLD): How does the animal model resemble human disease?

Despite decades of research, the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD) is still not completely understood. Based on the evidence from preclinical models, one of the factors proposed as a main driver of disease development is oxidative stress. This study aimed to search for the resemblance between the profiles of oxidative stress and antioxidant defense in theanimal model of MASLD and the group of MASLD patients. C57BL/6J mice were fed with the Western diet for up to 24 weeks and served as the animal model of MASLD. The antioxidant profile of mice hepatic tissue was determined by liquid chromatography-MS3 spectrometry (LC-MS/MS). The human cohort consisted of 20 patients, who underwent bariatric surgery, and 6 controls. Based on histological analysis, 4 bariatric patients did not have liver steatosis and as such were also classified as controls. Total antioxidant activity was measured in sera and liver biopsy samples. The hepatic levels of antioxidant enzymes and oxidative damage were determined by Western Blot. The levels of antioxidant enzymes were significantly altered in the hepatic tissue of mice with MASLD. In contrast, there were no significant changes in the antioxidant profile of hepatic tissue of MASLD patients, except for the decreased level of carbonylated proteins. Decreased protein carbonylation together with significant correlations between the thioredoxin system and parameters describing metabolic health suggest alterations in the thiol-redox signaling. Altogether, these data show that even though the phenotype of mice closely resembles human MASLD, the animal-to-human translation of cellular and molecular processes such as oxidative stress may be more challenging.

Investigation on Anti-diabetic Efficacy of a Cucurbitaceae Food Plant from the North-East Region of India: Exploring the Molecular Mechanism through Modulation of Oxidative Stress and Glycosylated Hemoglobin (HbA1c).

The medicinal plants of the Cucurbitaceae family, such as Solena heterophylla Lour. fruits, have significant ethnobotanical value and are readily accessible in North East India. We conducted a study on Solena heterophylla Lour. fruits to evaluate their anti-diabetic activity in vivo, standardize their HPTLC, and profile their metabolites using LC-QTOF-MS. We aimed to explore the molecular mechanism behind their effects on oxidative stress and glycosylated hemoglobin (HbA1c). Firstly, the ethyl acetate fraction of Solena heterophylla Lour. fruits was standardized using Cucurbitacin B as a standard marker by conducting HPTLC evaluation. Next, we delved into analyzing metabolite profiling. In addition, the standardized fraction was utilized in an experimental study to investigate the molecular mechanism of action in an in vivo high-fat diet and a low dose of streptozotocin-induced diabetic model. We have reportedly identified 52 metabolites in the ethyl acetate fraction of Solena heterophylla (EASH). In the in vitro tests, it has been observed that this extract from plants possesses notable inhibitory properties against α-amylase and α-glucosidase. Solena heterophylla fruits with high levels of Cucurbitacin B (2.29% w/w) helped lower FBG levels in animals with EASH treatment. EASH treatment reduced HbA1c levels and normalized liver lipid peroxidation and antioxidant enzyme levels. SGOT, SGPT, and SALP serum enzyme levels also returned to normal. Based on the current evaluation, it was found that EASH exhibited encouraging hypoglycemic effects in diabetic rats induced by a low dose of STZ and high-fat diet, which warrants further investigation.

Hepatoprotective effect of methanol fruit extract of Punica granatum L in highly active antiretroviral therapy-induced toxicity in Wistar rats

Prolonged use of Highly Active Antiretroviral Therapy (HAART) has been linked to toxicity, particularly hepatotoxicity. There are few effective drugs for HAART patients that promote hepatic cell regeneration and prevent liver injury. Therefore, the purpose of this study was to investigate the hepato-protective activity of Methanol fruit extract of Punica granatum (MFEPG) in HAART-administered rats. Thirty rats weighing between 150–200 g were randomly divided into six groups and each group comprised of five rats. Distilled water was given to the rats in group one. Only HAART was given to the rats in group two. MFEPG at doses of 100 and 400 mg/kg was given to the rats in groups three and four. MFEPG dosages of 100 and 400 mg/kg along with HAART were given to the rats in groups five and six, respectively. All treatments were via oral gavage daily for 40 days. Under halothane anesthesia, all rats were sacrificed on day 41. Liver tissues were utilized for lipid peroxidation marker; Malondialdehyde (MDA), antioxidant enzymes; Superoxide dismutase (SOD) and Catalase (CAT) and histological evaluation, while blood samples were examined for biochemical parameters (AST, ALT, ALP, Total cholesterol, Total protein, and Albumin). The HAART-treated group exhibited a significantly higher amount of the lipid peroxidation end product; MDA, and significantly lower levels of antioxidant enzymes; SOD, and CAT. Liver enzymes and total cholesterol were significantly increased with a significant reduction in Total protein and Albumin levels in the HAART-treated group. Conversely, the liver function biomarkers were returned to normal levels in the HAART and MFEPG-treated groups. Histopathological studies revealed that when HAART-exposed rats were treated with MFEPG, both the biochemical and histological results significantly improved. Thus, the antioxidant activity of MFEPG provides protection against HAART-induced liver oxidative damage. More research is needed to determine the safety of using MFEPG in humans.

Efficacy of Jiuzao polysaccharides in ameliorating alcoholic fatty liver disease and modulating gut microbiota

Jiuzao, the residue from Baijiu production, has shown radical scavenging properties in prior investigations, suggesting its potential as a hepatoprotective agent against acute liver damage. This study reveals that Jiuzao polysaccharides ameliorated liver morphological damage in zebrafish larvae afflicted with alcoholic fatty liver disease (AFLD), as evidenced by Oil red O, H&E, and Nile red staining. These polysaccharides notably modulated antioxidant enzyme levels and lipid peroxidation components. The real-time quantitative polymerase chain reactions analyses illustrated the significant impact of Jiuzao polysaccharides on genes integral to ethanol and lipid metabolism. The 16 S rRNA results showed that Jiuzao polysaccharides could improve the intestinal flora in zebrafish larvae exposed to ethanol. In summary, Jiuzao polysaccharides efficaciously mitigate liver lipid accumulation, enhance ethanol metabolism, and reduce oxidative stress by downregulating genes involved in AFLD development. They also regulate the changes in gut microbiota, providing further protection against acute alcoholic liver insult in zebrafish larvae.

Boosting cadmium tolerance in Phoebe zhennan: the synergistic effects of exogenous nitrogen and phosphorus treatments promoting antioxidant defense and root development.

Plants possess intricate defense mechanisms to resist cadmium (Cd) stress, including strategies like metal exclusion, chelation, osmoprotection, and the regulation of photosynthesis, with antioxidants playing a pivotal role. The application of nitrogen (N) and phosphorus (P) fertilizers are reported to bolster these defenses against Cd stress. Several studies investigated the effects of N or P on Cd stress in non-woody plants and crops. However, the relationship between N, P application, and Cd stress resistance in valuable timber trees remains largely unexplored. This study delves into the Cd tolerance mechanisms of Phoebe zhennan, a forest tree species, under various treatments: Cd exposure alone, combined Cd stress with either N or P and Cd stress with both N and P application. Our results revealed that the P application enhanced root biomass and facilitated the translocation of essential nutrients like K, Mn, and Zn. Conversely, N application, especially under Cd stress, significantly inhibited plant growth, with marked reductions in leaf and stem biomass. Additionally, while the application of P resulted in reduced antioxidant enzyme levels, the combined application of N and P markedly amplified the activities of peroxidase by 266.36%, superoxide dismutase by 168.44%, and ascorbate peroxidase by 26.58% under Cd stress. This indicates an amplified capacity of the plant to neutralize reactive oxygen species. The combined treatment also led to effective regulation of nutrient and Cd distribution in roots, shoots, and leaves, illustrating a synergistic effect in mitigating toxic impact of N. The study also highlights a significant alteration in photosynthetic activities under different treatments. The N addition generally reduced chlorophyll content by over 50%, while P and NP treatments enhanced transpiration rates by up to 58.02%. Our findings suggest P and NP fertilization can manage Cd toxicity by facilitating antioxidant production, osmoprotectant, and root development, thus enhancing Cd tolerance processes, and providing novel strategies for managing Cd contamination in the environment.

Siderophore of plant growth promoting rhizobacterium origin reduces reactive oxygen species mediated injury in Solanum spp. caused by fungal pathogens.

The study aims to explore antifungal properties of bacillibactin siderophore produced by the plant growth-promoting rhizobacterium (PGPR) Bacillus subtilis against fungal phytopathogens Alternaria porri and Fusarium equiseti isolated from Solanum lycopersicum and Solanum melongena plants. Alternaria porri and F. equiseti were isolated from infected plants of eggplant and tomato, respectively. A plate assay was employed to assess the effect of bacillibactin against the phytopathogens. The antifungal potential of the PGPR was evaluated by estimation of dry fungal biomass, visualization of cellular deformity using compound and scanning electron microscopy, antioxidative enzyme assay and analysis of membrane damage via using lipid peroxidation. Inductively coupled plasma atomic emission spectroscopy (ICP-AES) analysis was employed to investigate changes in intracellular iron content. The impact of bacillibactin on pathogenesis was evaluated by infecting detached leaves of S. lycopersicum and S. melongena plants with both the pathogens and treating the infected leaves with bacillibactin. Leaves were further investigated for ROS accumulation, extent of necrosis and cell death. Our findings revealed significant damage to the hyphal structure of A. porri and F. equiseti following treatment with bacillibactin. Biomass reduction, elevated antioxidative enzyme levels, and membrane damage further substantiated the inhibitory effects of the siderophore on fungal growth. ICP-AES analysis indicates an increase in intracellular iron content suggesting enhanced iron uptake facilitated by bacillibactin. Moreover, application of 1500µg ml-1 bacillibactin on infected leaves demonstrated a substantial inhibition of ROS accumulation, necrosis, and cell death upon bacillibactin treatment. This study confirms the potent antagonistic activity of bacillibactin against both the phytopathogens A. porri and F. equiseti growth, supporting its potential as a promising biological control agent for fungal plant diseases. Bacillibactin-induced morphological, physiological, and biochemical alterations in the isolated fungi and pathogen-infected leaves highlight the prospects of bacillibactin as an effective and sustainable solution to mitigate economic losses associated with fungal infections in vegetable crops.

Macular pigments produced from microalga Chlorella sp. and applied to alleviate the pathogenic process in diabetic mice

Macular pigments (MP), which consist of lutein and zeaxanthin, have antioxidant capabilities and are widely used in eye healthcare. However, few studies have focused on the protective mechanisms of MP against diabetes mellitus. In addition, the advantages of MP produced by microalgae include non-competition with grains for land, year-round harvesting, and rapid growth. Therefore, this study aims to investigate the MP produced and extracted from the microalga Chlorella sp. AT1 and assess its impact on mitigating retinopathy and atherosclerotic damage in diabetic apolipoprotein E-deficient mice (ApoE−/−) subjected to high-fat diet and streptozotocin treatment. The results showed that the major components of MP were lutein and zeaxanthin in a 5:1 ratio. MP supplementation significantly reduced glucose tolerance and insulin resistance by 25 and 41 %, respectively, in comparison to the diabetic group. MP supplementation resulted in the moderation of various inflammatory cytokines and lowered the serum levels of disease markers in comparison to the control group. In addition, the expression levels of cellular antioxidant enzymes were significantly elevated, aligning with a reduction in lipid peroxidation after MP supplementation, in comparison to the diabetic group. Pathological changes in the outer nuclear layer and aortic plaques in diabetic ApoE−/− mice were significantly alleviated by MP supplementation. In summary, microalgal MP alleviated the symptoms of type 2 diabetes mellitus in the diabetic ApoE−/− mice. Consequently, MP holds the potential to serve as a beneficial ingredient in healthy food, contributing to biological efficacy by scavenging free radicals and stabilizing blood glucose levels.

Evaluating Impacts of Biosynthetic Silver Nanoparticles on Morphophysiological Responses in Barley (Hordeum vulgare L.)

In recent years, nanotechnology has shown promising potential to enhance sustainable agriculture. Besides their use as antifungal and antimicrobial agents, silver nanoparticles (AgNPs) are the most widespread nanomaterials and are found in a capacious range of agrocommercial products. This study was designed to investigate the responses of morphophysiological characteristics in barley (Hordeum vulgare L.) to biologically synthesized silver nanoparticles. Spherical shapes with 8–20 nm size AgNPs at different concentrations (0, 50, 100, 150, 200, and 250 mg/L) were applied to barley plants in a hydroponic system. Following 7 days of sowing, the growth performance, chlorophyll contents, oxidative damage, and the activity level of antioxidant enzymes were quantified in different parts of the plant. The results indicated a remarkable boost in the growth performance and chlorophyll contents of barley plants up to a concentration of 150 mg/L. Interestingly, the levels of proline, lipid peroxidation, enzymes; superoxide dismutase (SOD), catalase (CAT), (APX), and (GR) activities were enhanced significantly in response to all AgNPs treatments. In general, the application of AgNPs substantially improved the growth and related morphophysiological attributes in barley. Our results provide new insights with respect to the effects of AgNPs on barley growth and their potential applications in increasing the performance of other crop species.

Melatonin Application Induced Physiological and Molecular Changes in Carnation (Dianthus caryophyllus L.) under Heat Stress

Carnation is one of the most important ornamental plants worldwide; however, heat stress is a problem, which affects carnation cultivation. The harmful effects of heat stress include impaired vegetative development and reduced floral induction. In this study, to enhance carnation growth under conditions of heat stress, various concentrations of melatonin were added to in vitro culture media. The mechanism by which melatonin reduced heat stress damage was then studied by taking measurements of morphological parameters, levels of reactive oxygen species (ROS), antioxidant enzymes, and malondialdehyde (MDA), as well as differential gene expression, in carnation plants during in vitro culture. These data revealed that untreated carnation plants were more harmed by conditions of heat stress than plants treated with melatonin. Melatonin at concentrations of 5 and 10 mM increased chlorophyll content, fresh weight, and plant height to a greater extent than other concentrations. Melatonin may, thus, be used to alleviate damage to carnations caused by heat stress. The application of melatonin was also found to reduce oxidative damage and enhance antioxidant defense mechanisms. In addition, the expression of heat-related genes was found to be upregulated; in melatonin-treated plants, an upregulation was recorded in the expression of GAPDH, DcPOD1, DcPOD2, DcPOD3, Gols1, MBF1c, HSF30, HSP101, HSP70, and sHSP (MT) genes. In short, we found that melatonin treatment increased heat tolerance in carnation plants. The data presented here may serve as a reference for those seeking to enhance the growth of plants in conditions of heat stress.

ENHANCED MITOCHONDRIAL BIOGENESIS INCREASES ANTI-OXIDANT ENZYMES AND IMPROVES TISSUE INFLAMMATION IN HUMAN IBD TISSUE

Abstract BACKGROUND In patients with inflammatory bowel disease (IBD), there exists a connection between mitochondrial dysfunction and two key issues: increased oxidative stress and attenuated ATP production. Previously we presented at this meeting the effect of a novel gold-based compound (AuPhos) on enhancing mitochondrial function in attenuating mice colitis (). In the present study we interrogate the effect of AuPhos on mitochondrial biogenesis in biopsies from control and active ulcerative colitis (UC) (Mayo 1-2) patients and normal human colonic epithelial cells (NCM460). We postulate that AuPhos-induced mitochondrial function enhances biogenesis and anti-oxidant levels and improves tissue inflammation in human IBD tissue. METHODS Effects of AuPhos on mitochondrial and anti-oxidant proteins were evaluated in NCM460 cells by western blot (WB) +/- low-dose TNF(1ng/ml). Human colonic biopsy samples (n=3) were collected and treated ex-vivo with vehicle or AuPhos (3h, 4oC), and processed for protein and mRNA analysis by WB and RT-qPCR, respectively. Flow cytometry of mitotracker green quantified mitochondrial mass in NCM460 and intestinal epithelial cells (IECs) from human control and UC tissues (n=3, Mayo 1-2). RESULTS AuPhos increased mitochondrial mass (mitotracker, Fig.1A,1B) and biogenesis protein levels PGC1α, NRF2 and TFAM (Fig.1C) in human intestinal epithelial cells (IECs), biopsies, and in NCM460 cells. Protein analysis in NCM460 cells show that AuPhos increases downstream antioxidant markers such as manganese superoxide dismutase (MnSOD), glutathione peroxidase 4 (GPX4), thioredoxin reductase2 (Trx2), and catalase expression when compared to the TNF or control samples. AuPhos substantially upregulates levels of mitochondria complex (mtCO1, mtCO2 Cox6A1, ATP5A1) and anti-oxidant enzyme (MnSOD, GPX, PRDX-2, -4, and -6) mRNA and protein levels in human colonic biopsies compared to vehicle and TNF treated samples (Fig. 1D). Furthermore, AuPhos reduces tissue cytokine and chemokine mRNA levels (IL1β, MCP1, RankL, and TNFα) in human UC tissues (Fig. 1E). CONCLUSIONS The current study reveals that AuPhos increases mitochondrial biogenesis, mitochondrial complex, and antioxidant enzyme levels in human IBD tissue. THE REDUCTION IN TISSUE CYTOKINES AND CHEMOKINES SUGGESTS THAT ENHANCED MITOCHONDRIAL FUNCTION IMPROVES TISSUE INFLAMMATION. This suggests the potential of AuPhos in treating IBD through the restoration of mitochondrial biogenesis.