Increased Superoxide Dismutase Activity Research Articles

Impact of Pterostilbene on Lens Epithelial Cells from Cataract Model Rats

Lens epithelial cell (lEC) membrane is one of the pathological process of cataract. Sandalwood stilbene is a kind of non-flavonoid polyphenol extracted from blueberries, grapes and other berries. It is considered as a natural antioxidant through various related mechanisms. This study was to investigate the effect and mechanism of Rosewood astragalus on lEC in oxidative cataract rats, and to provide evidence for clinical cataract treatment. Grouping method: normal control group, model group (H2O2 induced cataract) and Zitan astragalus group. Lens turbidity was observed, LECs was isolated and cultured. MTT assay was used to detect LECs proliferation and Caspase-3 activity was used to detect LECs apoptosis. The expression of NF-κB pathway was analyzed. The activities of superoxide dismutase (SOD), reactive oxygen species (ROS) were detected. The results showed that H2O2 significantly increased lens turbidity, enhanced Caspase-3 activity, inhibited LECs proliferation, increased NF-κB pathway expression, increased ROS activity, and decreased SOD activity (P <0.05). Dansandalus stilbene had the effects of inhibiting NF-κB pathway expression, promoting LECs proliferation, decreasing Caspase-3 activity, decreasing ROS production and increasing SOD activity (P < 0.05). In this study, it is suggested that Rosewood stilbene delaying the oxidation of traumatic cataract by anti-oxidation and apoptosis of LECs, and regulating cell proliferation, inhibiting the expression of NF-κB.

Activation of SIRT3 by Tanshinone IIA ameliorates renal fibrosis by suppressing the TGF-β/TSP-1 pathway and attenuating oxidative stress.

Although doxorubicin (DOX) is a common chemotherapeutic drug, the serious nephrotoxicity caused by DOX-induced renal fibrosis remains a considerable clinical problem. Tanshinone IIA (Tan IIA), a compound extracted from Salvia miltiorrhiza, has been reported to have an anti-fibrotic effect. Therefore, this study investigated the molecular pathway whereby Tan IIA protects the kidneys from DOX administration. DOX (3mg/kg body weight) was intraperitoneally administered every 3 d for a total of 7 injections (cumulative dose of 21mg/kg) to induce nephrotoxicity. Then, Tan IIA (5 or 10mg/kg/d) was administered by intraperitoneal injection for 28 d. In an in vitro study, 293T cells were cultured and treated with DOX and Tan IIA for 24h. Tan IIA reduced the blood urea nitrogen levels elevated by DOX while increasing superoxide dismutase activity, down-regulating reactive oxygen species, ameliorating renal-tubule thickening, and rescuing mitochondrial morphology. Additionally, Tan IIA reduced the renal collagen deposition, increased ATP production and complex-I activity, down-regulated transforming growth factor-β1 (TGF-β1) and thrombospondin-1 (TSP-1), and up-regulated sirtuin 3 (SIRT3). Tan IIA significantly increased cell viability. Additionally, RNA interference was employed to silence the expression of SIRT3, which eliminated the effect of Tan IIA in suppressing the expression of TGF-β1 and TSP-1. In conclusion, Tan IIA ameliorated DOX-induced nephrotoxicity by attenuating oxidative injury and fibrosis. The Tan IIA-induced rescue of mitochondrial morphology and function while alleviating renal fibrosis may be associated with the activation of SIRT3 to suppress the TGF-β/TSP-1 pathway.

Microplastics and copper impacts on feeding, oxidative stress, antioxidant enzyme activity, and dimethylated sulfur compounds production in Manila clam Ruditapes philippinarum

Microplastics (MPs) are widespread ocean pollutants and many studies have explored their effects. However, research on MPs combined impact with copper (Cu) on dimethylated sulfur compound production is limited. Dimethyl sulfide (DMS) is an important biogenic sulfur compound related to global temperatures. This study examined the ecotoxicological effects of polyamide 6 MPs and Cu and dimethylsulfoniopropionate (DMSP), DMS, and dimethyl sulfoxide (DMSO) production in Manila clams (Ruditapes philippinarum). Our findings showed that MPs and Cu increased oxidative stress, indicated by higher superoxide anion radical production and malondialdehyde levels while decreasing glutathione contents and increasing superoxide dismutase activities. Additionally, MPs and Cu exposure reduced DMS, dissolved DMSP (DMSPd), and dissolved DMSO (DMSOd) concentrations due to decreased grazing. These results contribute to a better understanding of the ecotoxicological effects of MPs/Cu on bivalves and their roles in the organic sulfur cycle, suggesting a need for further research on long-term impacts on them.

Comparative analysis of cyto-genotoxicity of zinc using the comet assay and chromosomal abnormality test.

In this study, the toxicity of the trace element zinc (Zn) in Allium cepa L. test material was examined. Toxicity was investigated in terms of physiological, cytogenetic, biochemical, and anatomical aspects. Germination percentage, root length, weight gain, mitotic index (MI), micronucleus (MN) frequency, chromosomal abnormalities (CAs), malondialdehyde (MDA), proline and chlorophyll levels, superoxide dismutase (SOD) and catalase (CAT) enzyme activities, and meristematic cell damage were used as indicators of toxicity. Additionally, the comet test was used to measure the degree of DNA damage. Four groups of A. cepa bulbs-one for control and three for applications-were created. While the bulbs in the treatment groups were germinated with Zn at concentrations of 35, 70, and 140mg/L, the bulbs in the control group were germinated with tap water. Germination was carried out at room temperature for 72h and 144h. When the allotted time was over, the root tips and leaf samples were collected and prepared for spectrophotometric measurements and macroscopic-microscopic examinations. Consequently, Zn treatment led to significant reductions in physiological indicators such as weight gain, root length, and germination percentage. Zn exposure caused genotoxicity by decreasing the MI ratios and increasing the frequency of MN and CAs (p < 0.05). Zn promoted various types of CAs in root tip cells. The most observed of CAs was the sticky chromosome. Depending on the dose, Zn was found to cause an increase in tail lengths in comet analyses, which led to DNA damage. Exposure to Zn led to a significant decrease in chlorophyll levels and an increase in MDA and proline levels. It also promoted significant increases in SOD and CAT enzyme activities up to 70mg/L dose and statistically significant decreases at 140mg/L dose. Additionally, Zn exposure caused different types of anatomical damage. The most severe ones are epidermis and cortex cell damage. Besides, it was found that the Zn dose directly relates to all of the increases and decreases in physiological, cytogenetic, biochemical, and anatomical parameters that were seen as a result of Zn exposure. As a result, it has been determined that the Zn element, which is absolutely necessary in trace amounts for the continuation of the metabolic activities of the organisms, can cause toxicity if it reaches excessive levels.

Curcumin Prevents Renal Damage of l-NAME Induced Hypertension in by Reducing MMP-2 and MMP-9.

In the present study, we investigated whether curcumin administration would interfere with the main renal features of l-NAME-induced hypertension model. For this purpose, we conducted both in vitro and in vivo experiments to evaluate renal indicators of inflammation, oxidative stress, and metalloproteinases (MMPs) expression/activity. Hypertension was induced by l-NAME (70 mg/kg/day), and Wistar rats from both control and hypertensive groups were treated with curcumin (50 or 100 mg/kg/day; gavage) or vehicle for 14 days. Blood and kidneys were collected to determine serum creatinine levels, histological alterations, oxidative stress, MMPs expression and activity, and ED1 expression. l-NAME increased blood pressure, but both doses of curcumin treatment reduced these values. l-NAME treatment increased creatinine levels, glomeruli area, Bowman's space, kidney MMP-2 activity, as well as MMP-9 and ED1 expression, and reduced the number of glomeruli. Curcumin treatment prevented the increase in creatinine levels, MMP-2 activity, and reduced MMP-2, MMP-9, ED1, and superoxide levels, as well as increased superoxide dismutase activity and partially prevented glomeruli alterations. Moreover, curcumin directly inhibited MMP-2 activity in vitro. Thus, our main findings demonstrate that curcumin reduced l-NAME-induced hypertension and renal glomerular alterations, inhibited MMP-2 and MMP-9 expression/activity, and reduced oxidative stress and inflammatory processes, which may indirectly impact hypertension-induced renal outcomes.

Effect of different concentrations of inulin on ram sperm quality during cryopreservation

BACKGROUND: In reproductive biotechnology, sperm cryopreservation has a vital role to play. Cryopreservation of sperm produces reactive oxygen species (ROS), which disrupt sperm function and structural competence. Numerous protective chemicals, including fructans, have been used during sperm cryopreservation. OBJECTIVES: To evaluate the effect of different concentrations of the fructosan inulin on ram sperm quality parameters, superoxide dismutase (SOD) activity, and malondialdehyde (MDA) production after freezing and thawing. MATERIALS AND METHODS: The pooled samples from four healthy rams were divided into seven equal aliquots and diluted in a Tris-base extender supplemented with 1, 2, 4, 8, 16, and 28 mM of inulin or without inulin supplementation (control). By using liquid nitrogen vapor, the semen was frozen and stored at 196°C. RESULTS: The total motility, viability, and DNA integrity were significantly improved after freezet-hawing with 28 mM inulin, compared to other treatment groups (P&lt;0.05). A Tris-based extender containing 16 and 28 mM of inulin displayed the highest levels of ram sperm membrane integrity when compared with the control (p&lt;0.05). The abnormality of ram sperm was increased during freeze-thawing at control and 1 mM of inulin, compared to 16 and 28 mM of inulin (P&lt;0.05). Additionally, 28 mM of inulin decreased MDA and increased SOD activity in ram sperm in comparison with the other treatments (P&lt;0.05). CONCLUSION: As a result, 28 mM of inulin could be beneficial for the cryopreservation industry and reduce the harmful effects of freeze-thawing on ram sperm.

SPRY4 regulates ERK1/2 phosphorylation to affect oxidative stress and steroidogenesis in polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder in women of childbearing age. The role of Sprouty RTK Signaling Antagonist 4 (SPRY4) in ovarian function in PCOS was investigated herein focusing on its regulation of ERK1/2 phosphorylation. PCOS models were established in mice using dehydroepiandrosterone (DHEA). The expression levels of SPRY4 in ovarian tissues were analyzed through RT-qPCR and immunohistochemistry. SPRY4 knockdown was achieved via lentivirus, and its effects on endocrine function, ovarian morphology, oxidative stress, and ERK1/2 phosphorylation were evaluated. Afterwards, granulosa cells were isolated and treated with DHEA and ERK2 agonist tert-Butylhydroquinone. The impacts of ERK2 activation on the regulation of SPRY4 knockdown were assessed using ELISA, fluorescent probes, western blotting, and biochemical assays. SPRY4 knockdown normalized the estrous cycle, reduced serum levels of testosterone, anti-Müllerian hormone, and luteinizing hormone/follicle-stimulating hormone ratio, and improved ovarian morphology. Additionally, SPRY4 knockdown alleviated oxidative stress by decreasing reactive oxygen species and malondialdehyde levels while increasing superoxide dismutase activity. It also restored steroidogenic enzyme expression, which were disrupted by DHEA induction. In vitro, SPRY4 knockdown enhanced granulosa cell viability and reduced ERK1/2 phosphorylation, with tert-Butylhydroquinone reversing these effects and restoring oxidative stress and steroidogenesis disruptions. Together, SPRY4 modulates ERK1/2 phosphorylation to influence oxidative stress and steroidogenesis in PCOS. Targeting SPRY4 may provide novel therapeutic avenues for improving ovarian function and managing PCOS.

The Eliciting Effect of Aqueous Extracts from Ascophyllum nodosum Algae on the Cultivation of Arugula (Eruca sativa Mill.) Microgreens

This study showed the eliciting effect of aqueous extracts from Ascophyllum nodosum on the development of Eruca sativa microgreens in a quartz-based substrate. There is no information in the literature on the impact of its use on the quality, bioactive compound content, and nutritional value of arugula microgreens. Assays that have been made include the following: total phenolic content (TPC), total flavonoid content (TFV), enzymes such as phenylalanine ammonia (PAL) and polyphenol oxidase (PPO), and enzymes involved in the scavenging of reactive oxygen species such as catalase (CAT) and superoxide dismutase (SOD). The antioxidant activity against DPPH (2,2-diphenyl-1-picrylhydrazyl) was also evaluated. The total phenolic content of arugula microgreens increased significantly after an application of aqueous extracts of A. nodosum to the substrate. The greatest increase in flavonoid content (89%) and antioxidant activity against DPPH (82%) was observed at a concentration of 2.5%. The highest increase in activity of CAT (68.2%), SOD (25%), PAL (13-fold), and PPO (84.2%) was observed with the application of 5% extract. In conclusion, the use of Ascophyllum nodosum algae affects TPC and TFV, antioxidant activity, PAL, PPO, SOD, and CAT in the microgreens studied. By prioritising organic and environmentally friendly extracts, growers can contribute to a more sustainable and healthier food system, especially in the case of the production of Eruca sativa microgreens.

Exploring the impact of high salinity and parasite infection on antioxidant and immune systems in Coris julis in the Pityusic Islands (Spain)

Climate change associated with human activities alters marine ecosystems and causes imbalances and abrupt changes in sea conditions. Scarce freshwater resources for human consumption often prompt the construction of desalination plants, which discharge significant amounts of brine into the sea, potentially elevating salinity levels. Furthermore, global trade together with higher temperature and pollution can facilitate the spread of parasites. The aim of this study was to assess the potential effects of salinity, an abiotic stressor, and Scaphanocephalus sp. parasitic infection responsible for black spot disease, a biotic stressor, on Coris julis, a common fish in the Balearic Islands (Spain). Fish were sampled from an area affected by a desalination plant, one with a high rate of parasite infection and a control area, and biomarkers were analysed in the liver, gills and epithelial mucosa. Both salinity and the parasite induced increases in catalase (CAT) and glutathione s-transferase activities in the liver, while superoxide dismutase (SOD) did not show significant changes. The effects of salinity were evident to a greater extent in the gills with an increase in the activity of all enzymes, as well as in the production of reactive species. The effects of the parasite were mainly observed in the mucus with significant increases in CAT and SOD activities. Regarding immune response markers in the mucus, both stressors induced an increase in lysozyme and alkaline phosphatase activities, and in the case of the parasite, also an increase in immunoglobulins. Malondialdehyde, as an indicator of oxidative damage, remained unchanged. In conclusion, both abiotic and abiotic stress induce a stress situation in C. julis that responds by activating its antioxidant and immune defence mechanisms but does cause oxidative damage. The differential tissue response to different stressors highlights the value of analysing multiple tissues to detect early indicators of diverse impacts on marine fauna.

Effects of inorganic and organic pollution on development of Steindachneridion melanodermatum from the Iguaçu river, Brazil

The Iguaçu River basin, known for its rich endemic ichthyofauna, faces a significant threat from chemical pollution. The Jordão River, a major tributary, drains extensive agricultural and livestock areas and receives poorly treated domestic and industrial effluents before joining the Iguaçu River. This study investigated the pollution and toxic effects of water samples from the Iguaçu upstream (UI), Jordão (JR), and their confluence (DI) on Steindachneridion melanodermatum embryos and larvae. Chemical analyses of the water samples revealed that most contaminants were present at levels below detection limits or within the limits established by Brazilian legislation. However, cadmium in UI, aluminum in JR, and lead in DI exceeded the legal limits. Exposure up to 96 h post-fertilization revealed higher mortality and deformity rates in individuals exposed to water samples from UI and JR, despite JR having fewer detected pollutants. JR and DI samples induced increased superoxide dismutase activity, indicating activation of the antioxidant defense system due to xenobiotic exposure. Overall, the integrated biomarker response indexes showed that individuals exposed to JR water displayed the most significant variations in their responses compared to the control treatment, suggesting a higher level of contamination and toxicity. Although a direct link between water quality and toxicity in the Jordão and Iguaçu Rivers was inconclusive, the results confirmed pollution and risks to local wildlife. The study highlighted the harmful effects of pollutants, even at low concentrations. These findings underscore the need for conservation measures to safeguard endemic and endangered species in the Iguaçu River basin. Understanding pollutant effects on native species is crucial for effective mitigation strategies and ecological health preservation.

Exiguobacterium acetylicum Strain SI17: A Potential Biocontrol Agent against Peronophythora litchii Causing Post-Harvest Litchi Downy Blight

Litchi downy blight (LDB) caused by Peronophythora litchii destroys 20–30% of litchi fruit every year and causes significant economic losses. Some Exiguobacterium strains exhibit considerable promise in both agricultural and industrial sectors. E. acetylicum SI17, isolated from the litchi fruit carposphere, demonstrated significant biocontrol activity against LDB through pre-harvest treatment. To elucidate its underlying regulatory mechanisms, the genome of SI17 was sequenced and analyzed, revealing a circular chromosome spanning 3,157,929 bp and containing 3541 protein-coding genes and 101 RNA genes. Notably, 94 genes were implicated in the production of secondary metabolites. Among the 29 Exiguobacterium strains so far sequenced, SI17 possessed the largest genome. In the phylogenomic analysis encompassing the entire genome, SI17 was clustered into Group I. Treating litchi fruit with SI17 before harvesting resulted in a decrease in H2O2 content in the fruit peel and an increase in superoxide dismutase activity, thus enhancing resistance to LDB. Interestingly, SI17 did not display plate antagonism against Peronophythora litchii SC18. It can be inferred that SI17 generates secondary metabolites, which enhance litchi’s resistance to LDB. This study represents the first documentation of an Exiguobacterium strain exhibiting a role in litchi plant disease and showcasing significant potential for the biological control of LDB.

Berberine Inhibits Ferroptosis and Stabilizes Atherosclerotic Plaque through NRF2/SLC7A11/GPX4 Pathway.

To investigate potential mechanisms of anti-atherosclerosis by berberine (BBR) using ApoE-/- mice. Eight 8-week-old C57BL/6J mice were used as a blank control group (normal), and 56 8-week-old AopE-/- mice were fed a high-fat diet for 12 weeks, according to a completely random method, and were divided into the model group, BBR low-dose group (50 mg/kg, BBRL), BBR medium-dose group (100 mg/kg, BBRM), BBR high-dose group (150 mg/kg, BBRH), BBR+nuclear factor erythroid 2-related factor 2 (NRF2) inhibitor group (100 mg/kg BBR+30 mg/kg ML385, BBRM+ML385), NRF2 inhibitor group (30 mg/kg, ML385), and positive control group (2.5 mg/kg, atorvastatin), 8 in each group. After 4 weeks of intragastric administration, samples were collected and serum, aorta, heart and liver tissues were isolated. Biochemical kits were used to detect serum lipid content and the expression levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in all experimental groups. The pathological changes of atherosclerosis (AS) were observed by aorta gross Oil Red O, aortic sinus hematoxylin-eosin (HE) and Masson staining. Liver lipopathy was observed in mice by HE staining. The morphology of mitochondria in aorta cells was observed under transmission electron microscope. Flow cytometry was used to detect reactive oxygen species (ROS) expression in aorta of mice in each group. The content of ferrous ion Fe2+ in serum of mice was detected by biochemical kit. The mRNA and protein relative expression levels of NRF2, glutathione peroxidase 4 (GPX4) and recombinant solute carrier family 7 member 11 (SLC7A11) were detected by quantitative real time polymerase chain reaction (RT-qPCR) and Western blot, respectively. BBRM and BBRH groups delayed the progression of AS and reduced the plaque area (P<0.01). The characteristic morphological changes of ferroptosis were rarely observed in BBR-treated AS mice, and the content of Fe2+ in BBR group was significantly lower than that in the model group (P<0.01). BBR decreased ROS and MDA levels in mouse aorta, increased SOD activity (P<0.01), significantly up-regulated NRF2/SLC7A11/GPX4 protein and mRNA expression levels (P<0.01), and inhibited lipid peroxidation. Compared with the model group, the body weight, blood lipid level and aortic plaque area of ML385 group increased (P<0.01); the morphology of mitochondria showed significant ferroptosis characteristics; the serum Fe2+, MDA and ROS levels increased (P<0.05 or P<0.01), and the activity of SOD decreased (P<0.01). Compared with BBRM group, the iron inhibition effect of BBRM+ML385 group was significantly weakened, and the plaque area significantly increased (P<0.01). Through NRF2/SLC7A11/GPX4 pathway, BBR can resist oxidative stress, inhibit ferroptosis, reduce plaque area, stabilize plaque, and exert anti-AS effects.

Safflower Yellow Injection Alleviates Myocardial Ischemia/Reperfusion Injury by Reducing Oxidative and Endoplasmic Reticulum Stress.

Safflower yellow is an extract of the famous Chinese medicine Carthamus tinctorious L, and safflower yellow injection (SYI) is widely used clinically to treat angina pectoris. However, there are few studies on the anti-myocardial ischemia/reperfusion (I/R) injury effect of SYI, and its mechanisms are unclear. In the present study, we aimed to investigate the protective effect of SYI on myocardial I/R injury and explore its underlying mechanisms. Male Sprague Dawley rats were randomly divided into a control group, sham group, model group, and SYI group (20 mg/kg, femoral vein injection 1 h before modeling). The left anterior descending coronary artery was ligated to establish a myocardial I/R model. H9c2 cells were exposed to oxygen-glucose deprivation/reoxygenation (OGD/R) after incubation with 80 μg/mL SYI for 24 h. In vivo, TsTC, HE, and TUNEL staining were performed to evaluate myocardial injury and apoptosis. A kit was used to detect superoxide dismutase (SOD) and malondialdehyde (MDA) to assess oxidative stress. In vitro, flow cytometry was used to detect the reactive oxygen species (ROS) content and apoptosis rate. Protein levels were determined via Western blotting. Pretreatment with SYI significantly reduced infarct size and pathological damage in rat hearts and suppressed cardiomyocyte apoptosis in vivo and in vitro. In addition, SYI inhibited oxidative stress by increasing SOD activity and decreasing MDA content and ROS production. Myocardial I/R and OGD/R activate endoplasmic reticulum (ER) stress, as evidenced by increased expression of activating transcription factor 6 (ATF6), glucose-regulated protein 78 (GRP78), cysteinyl aspartate-specific proteinase caspase-12, and C/EBP-homologous protein (CHOP), which were all inhibited by SYI. SYI ameliorated myocardial I/R injury by attenuating apoptosis, oxidative damage, and ER stress, which revealed new mechanistic insights into its application.

INVESTIGATION OF METABOLIC DISORDERS IN VARIOUS ORGANS IN WATER-IMMERSION RESTRAINT STRESS IN RATS AND ITS CORRECTION WITH PHARMACEUTICALS

The aim of the study. To investigate the impact of L-arginine and diclofenac sodium on changes in the prooxidant-antioxidant balance in liver, spleen and lungs in water-immersion restraint stress in rats. Materials and methods. The study was conducted on 50 male rats weighing 180-240 g in accordance with the international bioethical principles. Water-immersion restraint stress (WIRS) was modeled according to the method of Takagi et al. Experimental animals were studied in five groups (n = 10 per group) as follows: (1) intact animals; (2) those in which WIRS was simulated; (3) animals receiving diclofenac sodium (40 mg/kg) per os 30 minutes before WIRS; (4) animals receiving L-arginine (10 mg/kg) per os 30 minutes before WIRS. For sample collection, the rats were deeply anesthetized (thiopental sodium, 40 mg/kg). The liver, spleen and lungs were isolated and homogenized. The state of antioxidant defense system was assessed by the activity of superoxide dismutase (SOD) and catalase (CAT). To evaluate the activity of prooxidative processes, the levels of thiobarbituric acid reactive substances (TBARS), oxidative protein modification (OPM) and middle mass molecules (MMM) were investigated. The statistical analysis was performed according to Student’s criterion, using Microsoft Excel 8.0 software. Differences were considered statistically significant at p&lt;0,05. Result. The development of WIRS led to the increase in the prooxidant processes intensity in liver: TBARS by 41%, OPM by 76%, MMM by 160%; in lungs: TBARS by 43%, OPM by 71%, MMM by 99%; in spleen: TBARS by 110%, OPM by 87%, MMM by 205%. When corrected with diclofenac sodium, a decrease in prooxidant processes was observed in the liver: TBARS by 27%, OPM by 48%, MMM by 34%; in the lungs: TBARS by 23%, OPM by 40%, MMM by 19%; in the spleen: TBARS by 28%, insignificant decrease in OPM, MMM by 37%. The activity of these processes decreased in all organs also when the condition was corrected with L-arginine, although less noticeably: in the liver: TBARS by 23%, OPM by 31%, MMM by 11%; in the lungs: TBARS by 14%, OPM by 19%, MMM by 11%; in the spleen: TBARS by 32%, no statistically significant decrease in OPM, MMM by 27%. The activity of antioxidant enzymes under the conditions of WIRS development abruptly decreased in the liver: SOD by 42% and CAT by 30%; in the lungs: SOD and CAT by 30%; in the spleen: SOD by 56%, CAT by 40%. The administration of diclofenac sodium led to an increase in the activity of these enzymes in the liver: SOD by 49%, CAT by 17%; in the spleen: SOD by 51%, CAT by 17%; no significant change in CAT; in the lungs: SOD by 17% and no significant change in CAT. The administration of L-arginine had less effect on the normalization of antioxidant enzyme activity. The activity of SOD increased by 20%, CAT – by 12% in the liver; in the lungs SOD and CAT did not increase reliably, only a tendency to increase was observed; in the spleen, the activity of SOD increased by 29%, and CAT by 15%. The combined effect of both drugs showed the best results: normalization of prooxidant processes was observed, only the level of endogenous intoxication remained slightly elevated in all studied organs. The activity of antioxidant enzymes coincided with the level of control indicators. The obtained result indicates the expediency of the combined use of the studied pharmaceuticals. Conclusions It was found that the greatest changes in the pro- and antioxidant balance under the influence of stress factors were observed in the spleen, slightly less distinct in the liver, and minor in the lungs of the studied animals. It was shown that diclofenac sodium at a dose of 40 mg/kg significantly reduced the level of prooxidant markers, manifested a normalizing effect on the activity of antioxidants in all studied organs of rats. The drug reliably increased the activity of SOD and contributed to the stabilization of catalase activity. The administration of L-arginine at a dose of 10 mg/kg under the same conditions was marked by a decrease in prooxidant processes, a significant increase in SOD activity in the liver and spleen, and a tendency to increase catalase and superoxide dismutase activity in the lungs of rats. The study revealed that the combination of the pharmaceuticals had the most significant effect on the state of pro- and antioxidant system, since the activity of SOD and catalase increased to the control group values, which was accompanied by a serious decrease in the level of prooxidant indicators to the control values.

Protective effects of fermented Rosa roxburghii Tratt juice against ethanol‑induced hepatocyte injury by regulating the NRF2‑AMPK signaling pathway in AML‑12 cells.

Alcohol‑related liver disease (ALD) is a major health concern worldwide. In recent years, there has been growing interest in natural products and functional foods for preventing and treating ALD due to their potential antioxidant and hepatoprotective properties. Rosa roxburghii Tratt, known for its rich content of bioactive compounds, has demonstrated promising health benefits, including anti‑inflammatory and antioxidant effects. Fermentation has been utilized as a strategy to enhance the bioavailability and efficacy of natural products. In the present study, using a mixture of Rosa roxburghii Tratt juice, lotus leaf extract and grape seed proanthocyanidins fermented by Lactobacillus plantarum HH‑LP56, a novel fermented Rosa roxburghii Tratt (FRRT) juice was discovered that can prevent and regulate ethanol‑induced liver cell damage. Following fermentation, the pH was significantly decreased, and the content of VC and superoxide dismutase (SOD) were significantly increased, along with a noticeable enhancement in hydroxyl and 2,2‑diphenyl‑1‑picrylhydrazyl free radical scavenging abilities. Alpha Mouse liver 12 cells were exposed to ethanol for 24 h to establish an in vitro liver cell injury model. The present study evaluated the effects of FRRT on cell damage, lipid accumulation and oxidative stress markers. The results revealed that FRRT pretreatment (cells were pre‑treated with 2.5 and 5 mg/ml FRRT for 2 h) significantly reduced lipid accumulation and oxidative stress in liver cells. Mechanistically, FRRT regulated lipid metabolism by influencing key genes and proteins, such as AMP‑activated protein kinase, sterol regulatory element binding transcription factor 1 and Stearyl‑CoA desaturase‑1. Furthermore, FRRT enhanced antioxidant activity by increasing SOD activity, glutathione and catalase levels, while reducing reactive oxygen species and malondialdehyde levels. It also reversed the expression changes of ethanol‑induced oxidative stress‑related genes and proteins. In conclusion, a novel functional food ingredient may have been discovered with extensive potential applications. These findings indicated that FRRT has antioxidant properties and potential therapeutic benefits in addressing ethanol‑induced liver cell damage through its effects on liver lipid metabolism and oxidative stress.

Metabolic effects of physical exercise on zebrafish (Danio rerio) fed a high-fat diet.

The present study aimed to establish zebrafish as an experimental model for investigations into obesity and physical exercise, as well as to assess the effects of these factors on metabolism. The experiment spanned twelve weeks, comprising a feeding trial during which the last four weeks incorporated a physical exercise protocol. This protocol involved placing fifteen animals in a five-liter aquarium, where they were subjected to swimming at an approximate speed of 0.08m/s for 30min daily. Throughout the experiment, histological analyses of visceral, subcutaneous, and hepatic adipose tissues were conducted, along with biochemical analyses of total cholesterol and its fractions, triglycerides, glucose, lactate, and alanine aminotransferase (ALT) levels. Additionally, oxidative stress markers, such as reactive oxygen species (ROS) levels, superoxide dismutase (SOD) activity, and catalase activity and the formation of thiobarbituric acid-reactive substances, were investigated. The results revealed that the group fed a high-fat diet exhibited an increase in ROS production and SOD activity. In contrast, the group administered the high-fat diet and subjected to physical exercise demonstrated a notable reduction in visceral adipocyte area, hepatic steatosis levels, ALT levels, and SOD activity. These findings indicate that physical exercise has a positive effect on obesity and oxidative stress in zebrafish, providing promising evidence for future investigations in this field.

Cereblon deficiency ameliorates carbon tetrachloride-induced acute hepatotoxicity in HepG2 cells by suppressing MAPK-mediated apoptosis.

The liver is vulnerable to various hepatotoxins, including carbon tetrachloride (CCl4), which induces oxidative stress and apoptosis by producing reactive oxygen species (ROS) and activating the mitogen-activated protein kinase (MAPK) pathway. Cereblon (CRBN), a multifunctional protein implicated in various cellular processes, functions in the pathogenesis of various diseases; however, its function in liver injury remains unknown. We established a CRBN-knockout (KO) HepG2 cell line and examined its effect on CCl4-induced hepatocellular damage. CRBN-KO cells exhibited reduced sensitivity to CCl4-induced cytotoxicity, as evidenced by decreased levels of apoptosis markers, such as cleaved caspase-3, and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities. CRBN deficiency enhanced antioxidant defense, with increased superoxide dismutase activity and glutathione ratios (GSH/GSSG), as well as reduced pro-inflammatory cytokine expression. Mechanistically, the protective effects of CRBN deficiency appeared to involve the attenuation of the MAPK-mediated pathways, particularly through decreased phosphorylation of JNK and ERK. Overall, these results suggest the crucial role of CRBN in mediating the hepatocellular response to oxidative stress and inflammation triggered by CCl4 exposure, offering potential clinical implications for liver injury in a wide range of liver diseases.

Lovastatin Combination Therapy Increases the Survival and Proliferation of Rat Bone Marrow-Derived Mesenchymal Stem Cells Against the Inflammatory Activity of Lipopolysaccharide.

Oxidative stress hurts the survival of transplanted mesenchymal stem cells (MSCs). Lipopolysaccharide (LPS) preconditioning inhibits apoptotic death in MSCs. Also, Lovastatin's protective effect was reported on MSCs. Here, we investigated the potential of LPS and Lovastatin combination therapy on the survival and proliferation of MSCs. MSCs harvested from adult rats (240-260 g) femur and tibia bone marrow. Third passage MSCs were divided into 6 groups control group, LPS, LPS + Lovastatin (10 and 15 µM), and Lovastatin (10 and 15 µM). Cell survival and proliferation were assessed using an MTT assay 24 h after LPS, Lovastatin, or LPS + Lovastatin treatment. Also, Malondialdehyde (MDA) as a lipid peroxidation marker and antioxidant enzymes such as Glutathione peroxidase (GPX) and Superoxide dismutase (SOD) activity levels evaluated. Finally, the expression level of tumor protein P53 (P53) and octamer-binding transcription factor 4 (OCT4) genes were measured by qRT-PCR test. Lovastatin 10 μM potentiated proliferation and survival of MSCs. It can increase the activity of GPX and SOD. 10 µM Lovastatin could not affect MDA amounts but decreased the expression levels of P53 and Oct4 significantly. Nevertheless, treatment with LPS reduced the survival and proliferation of MSCs, along with a significant reduction in GPX activity. LPS + Lovastatin could increase SOD activity, however, GPX enzyme activity and MSCs proliferation did not change so, and it was not effective. We propose Lovastatin at the dose of 10 µM as a suitable combination agent to increase the survival and proliferation of MSCs in oxidative stress conditions.

Ripe Musa sapientum Peels Exhibit Neuroprotection Against Lead Acetate-Induced Brain Damage in Wistar Rats

Objective: Human health has continued to be at risk from lead exposure. This study explored the antioxidative potential of ethanol extract of ripe Musa sapientum peels to protect against lead acetate-induced neuronal insult in female wistar rats. Methods: Thirty adult female rats (120-160 g) were randomly divided into six groups (n = 5): Group 1 (control group) received 10 mL/kg of distilled water; Group 2 received 100 mg/kg lead acetate. Group 3 received 2.5 mg/kg of donepezil. Groups 4 to 6 received 100, 200, and 400 mg/kg ethanol extract of ripe M sapientum, respectively, via oral gavage. Groups 2 to 5 were co-treated with 100 mg/kg lead acetate for 21 days. Neurobehavioral parameter, biochemical and histological analyses of the hippocampus were determined. Recognition memory was evaluated using Novel Object Recognition Test. Results: There was a significant ( p &lt; 0.05) increase in total exploration, discrimination index, and percentage alternation in the ethanol extract M sapientum-treated groups compared with the lead acetate-induced group. M sapientum ethanol extract and dopamine significantly ( p &lt; 0.05) reduced acetylcholinesterase enzyme (AChE) and malondialdehyde (MDA) activities in a dose-dependent manner and significantly ( p &lt; 0.05) increased superoxide dismutase activity (SOD) dose dependently, respectively. In the histopathological analysis of the hippocampal area, there were mild vacuolation (V), mild degeneration as well as mild granular cell atrophy in the treated groups, suggesting that M sapientum may have neuroprotective properties. Conclusion: Ethanol extract of ripe M sapientum peels enhanced cognitive functions and may be beneficial in preventing neurodegenerative disorders via antioxidant mechanism.

Impact of ocean acidification on microzooplankton grazing dynamics

This study examines the potential impacts of projected atmospheric carbon dioxide (pCO2) levels reaching 800 ppm by the end of the century, focusing on ocean acidification effects on marine ecosystems in the coastal areas of Bohai. We investigated how acidification affects the grazing patterns of microzooplankton using dilution techniques and ecophysiological methods. Our findings indicate that acidic conditions shift the phytoplankton community structure, changing dominant species. Elevated CO2 concentrations reduced grazing pressure on phytoplankton, with less steep declines in growth rates at 800 ppm CO2 (spring: 2.43 d−1 vs. 2.16 d−1, summer: −0.46 d−1 vs. −0.73 d−1, autumn: −0.45 d−1 vs. −0.90 d−1) and significant decreases in grazing pressure percentages (%Pp from 0.84 to 0.58 and %Pi from 0.64 to 0.46). Short-term acid exposure significantly increased superoxide dismutase activity in both microplankton (from 0.03 to 0.08 U mg−1, p&amp;lt;0.01) and nanoplankton (from 0.05 to 0.09 U mg−1, p&amp;lt;0.001), indicating an adaptive response to oxidative stress. These results highlight that elevated CO2 levels primarily boost phytoplankton growth by reducing microzooplankton grazing pressure, resulting in higher growth rates and a shift towards smaller-sized phytoplankton, reflecting complex short-term ecological responses to acidification. Further research is needed to understand the long-term effects of ocean acidification on microzooplankton and their role in marine secondary productivity.