Biodegradable MoSe 2 @polyvinylpyrrolidone Nanoparticles With Multi-enzyme Activity for Ameliorating Acute Pancreatitis

Exogenous antioxidant materials mimicking endogenous antioxidant systems are commonly used for the treatment of oxidative stress-induced injuries. Thus, artificial enzymes have emerged as promising candidates for balancing and treating the dysregulation of redox homeostasis in vivo. Herein, a one-pot hydrothermal strategy for the facile preparation of MoSe2@polyvinylpyrrolidone (PVP) nanoparticles (NPs) is reported. The synthesized NPs were biodegradable due to their exposure to oxygen and exhibited high stability. Moreover, they effectively mimicked various naturally occurring enzymes (including catalase, superoxide dismutase, peroxidase, and glutathione peroxidase) and scavenged free radicals, such as 3-ethylbenzothiazoline-6-sulfonic acid, ·OH, ·O2−, and 1,1-diphenyl-2-picrylhydrazyl radical. Further apoptosis detection studies revealed that MoSe2@PVP NPs significantly increased the cell survival probability in H2O2 in a concentration-dependent manner. The cytoprotective effect of MoSe2@PVP NPs was explored for an animal model of acute pancreatitis, which confirmed its remarkable therapeutic efficacy. Owing to the biodegradable and biocompatible nature of MoSe2@PVP NPs, the findings of this work can stimulate the development of other artificial nanoenzymes for antioxidant therapies.

Nitrite Stress Induces Oxidative Stress and Leads to Muscle Quality Decreased in Wuchang Bream (Megalobrama amblycephala Yih) Juveniles

To determine the effects of nitrite exposure on muscle quality and physiological functions in Wuchang bream (Megalobrama amblycephala), we exposed M. amblycephala juveniles to acute nitrite (0, 1, 5, 10, 20 mg/L), and the muscle and blood samples were measured at 12, 24, 48, and 96 h. The results showed that when exposed to nitrite for 12 h, the concentrations of blood glucose, cortisol, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) in the 20 mg/L experimental group had the maximum value. The activity of lactate dehydrogenase (LDH) increased significantly in a dose-dependently manner and peaked at 96 h in the 20 mg/L group. During 96 h of exposure to nitrite, the total antioxidant capacity (T-AOC) and catalase (CAT) activity in the liver of the 20 mg/L experimental group were significantly higher than those of the control group, while the concentration of muscle glycogen showed a downtrend. At 12 h and 96 h, the hardness of the four experimental groups were significantly higher than that of the control group. Our research shows that acute sodium nitrite exposure will not only cause oxidative stress and decreased muscle quality in M. amblycephala juveniles but also will be accompanied by changes in serum biochemical index, liver antioxidant capacity, muscle physiological characteristics, and muscle physical characteristics. Preliminary speculation may be that acute nitrite exposure may cause M. amblycephala juveniles to choose to reduce muscle quality and activate antioxidant systems.

Contrasting effects of accumulation and tolerance characteristics in Arabidopsis thaliana under Cr(III) and Cr(VI) stress

In this study, for the first time we investigated Cr(III) and Cr(VI) stress-induced physiological and biochemical responses in Arabidopsis thaliana . The capacity of A. thalian to accumulate Cr is closely related to the valence of chromium. Cr(VI) was more toxic than Cr(III) as indicated by chromium accumulation and growth inhibition. When the concentration of chromium is greater than 200μM, the root length and biomass of A. thaliana are reduced. But interestingly, Cr(III) at 200μM increased the root length and biomass of A. thaliana compared to the control. The transmission electron microscope shows that Cr(VI) can cause the chloroplasts damaged and the chlorophyll reduced more than Cr(III). The chloroplasts were filled the starch grains. An increase of lipid peroxidation in A. thaliana roots caused by Cr was measured, and this effect increases as the increasing Cr. It indicated that A. thaliana suffers from Cr-induced oxidative stress which resulted cell death in roots. To fight against oxidative stress, Ascorbate peroxidase and Glutathione reductase were activated by Cr in antioxidant defense. The inhibition of growth, the accumulation of chromium, the responses of antioxidant systems, and the ultra-morphological changes indicate that Cr(VI) was more toxic than Cr(III) .

Inflammation, Oxidative Stress, Senescence in Atherosclerosis: Thioredoxine-1 as an Emerging Therapeutic Target

Atherosclerosis is a leading cause of cardiovascular diseases (CVD) worldwide and intimately linked to aging. This pathology is characterized by chronic inflammation, oxidative stress, gradual accumulation of low-density lipoproteins (LDL) particles and fibrous elements in focal areas of large and medium arteries. These fibrofatty lesions in the artery wall become progressively unstable and thrombogenic leading to heart attack, stroke or other severe heart ischemic syndromes. Elevated blood levels of LDL are major triggering events for atherosclerosis. A cascade of molecular and cellular events results in the atherosclerotic plaque formation, evolution, and rupture. Moreover, the senescence of multiple cell types present in the vasculature were reported to contribute to atherosclerotic plaque progression and destabilization. Classical therapeutic interventions consist of lipid-lowering drugs, anti-inflammatory and life style dispositions. Moreover, targeting oxidative stress by developing innovative antioxidant agents or boosting antioxidant systems is also a well-established strategy. Accumulation of senescent cells (SC) is also another important feature of atherosclerosis and was detected in various models. Hence, targeting SCs appears as an emerging therapeutic option, since senolytic agents favorably disturb atherosclerotic plaques. In this review, we propose a survey of the impact of inflammation, oxidative stress, and senescence in atherosclerosis; and the emerging therapeutic options, including thioredoxin-based approaches such as anti-oxidant, anti-inflammatory, and anti-atherogenic strategy with promising potential of senomodulation.

Biochar and Chitosan Regulate Antioxidant Defense and Methylglyoxal Detoxification Systems and Enhance Salt Tolerance in Jute (Corchorus olitorius L.)

We investigated the role of biochar and chitosan in mitigating salt stress in jute (Corchorus olitorius L. cv. O-9897) by exposing twenty-day-old seedlings to three doses of salt (50, 100, and 150 mM NaCl). Biochar was pre-mixed with the soil at 2.0 g kg−1 soil, and chitosan-100 was applied through irrigation at 100 mg L−1. Exposure to salt stress notably increased lipid peroxidation, hydrogen peroxide content, superoxide radical levels, electrolyte leakage, lipoxygenase activity, and methylglyoxal content, indicating oxidative damage in the jute plants. Consequently, the salt-stressed plants showed reduced growth, biomass accumulation, and disrupted water balance. A profound increase in proline content was observed in response to salt stress. Biochar and chitosan supplementation significantly mitigated the deleterious effects of salt stress in jute by stimulating both non-enzymatic (e.g., ascorbate and glutathione) and enzymatic (e.g., ascorbate peroxidase, dehydroascorbate reductase, monodehydroascorbate reductase, glutathione reductase superoxide dismutase, catalase, peroxidase, glutathione S-transferase, glutathione peroxidase) antioxidant systems and enhancing glyoxalase enzyme activities (glyoxalase I and glyoxalase II) to ameliorate reactive oxygen species damage and methylglyoxal toxicity, respectively. Biochar and chitosan supplementation increased oxidative stress tolerance and improved the growth and physiology of salt-affected jute plants, while also significantly reducing Na+ accumulation and ionic toxicity and decreasing the Na+/K+ ratio. These findings support a protective role of biochar and chitosan against salt-induced damage in jute plants.

The state of pro- and antioxidant systems in rats with DMH-induced colon carcinogenesis on the background of extracorporeal detoxification

Aim: Cancer is one of the leading causes of death in the world. The aim of this research was to study the indices of pro- and antioxidant systems in rats with dimethylhydrazine (DMH)-induced colon carcinogenesis on the background of the enterosorbent AUT-M use. Materials and methods: The study was performed on 70 white male rats weighing 200–250 g. Adenocarcinoma of the colon was simulated by subcutaneous injection of the DMH (Sigma-Aldrich Chemie, Japan) at a dose of 7.2 mg/kg once a week during 7 months. Enterosorbent AUT-M was administered intragastrically daily for 21 days after simulation of carcinogenesis at a dose of 1 ml of suspension per 100 g of animal body weight. The state of the pro- and antioxidant systems was studied by the content of oxidative modification of proteins products (OMP), the activity of superoxide dismutase (SOD), catalase (CAT), contents of ceruloplasmin (CP) and reduced glutathione (GSH). Results: It was found that DMH-induced colon carcinogenesis in rats is accompanied by disorders in the antioxidant defense system and activation of free radical oxidation processes. Enterosorbent AUT-M provides a significant reduction in the content of OMP370 and OMP430 in both blood serum and liver homogenate of rats. Moreover, the use of enterosorbent AUT-M demonstrated a significant increase in the activity of SOD, CAT, content of GSH and a decrease in CP content in investigated tissues. Conclusion: The use of enterosorbent AUT-М demonstrated prominent potential suppression for oxidative stress and positive effect on antioxidant defense system in rats with DMH-induced colon carcinogenesis.

Response of enzymatic and non-enzymatic antioxidant systems in Excoecaria agallocha to salt stress

The effect of NaCl stress on antioxidant enzymes activities was investigated in the leaves of Excoecaria agallocha. Plants were subjected to different levels of NaCl. 100 to 1000 mM. Above 500 mM these mangrove seedlings did not survive. The leaves of 60 day old plants were used for the analysis of enzyme activities. Parameters of enzymatic and non enzymatic antioxidants such as catalase (CAT), peroxidase (POD), ascorbate peroxidase (APX), polyphenol oxidase (PPO), superoxide dismutase (SOD), ascorbic acid (ASA) and alpha tocopherol were determined. The highest CAT, POD, APX, PPO and SOD activities in the leaf and root enhanced gradually up to 300 mM of NaCl, the highest ASA and tocopherol activities in the leaf and root were observed at 500 mM of NaCl. These data suggest that the capacity to limit oxidative damage is important for the salt tolerance of E. agallocha.

Mitochondrial Oxidative Stress—A Causative Factor and Therapeutic Target in Many Diseases

The excessive formation of reactive oxygen species (ROS) and impairment of defensive antioxidant systems leads to a condition known as oxidative stress. The main source of free radicals responsible for oxidative stress is mitochondrial respiration. The deleterious effects of ROS on cellular biomolecules, including DNA, is a well-known phenomenon that can disrupt mitochondrial function and contribute to cellular damage and death, and the subsequent development of various disease processes. In this review, we summarize the most important findings that implicated mitochondrial oxidative stress in a wide variety of pathologies from Alzheimer disease (AD) to autoimmune type 1 diabetes. This review also discusses attempts to affect oxidative stress as a therapeutic avenue.