Indicator Of Oxidative Damage Research Articles

Hormonal signaling regulates photosynthetic function of alfalfa (Medicago sativa L.) under NaHCO3 stress

The physiological and molecular mechanisms underlying salt-alkali tolerance in Medicago sativa are of significant importance for the development of animal husbandry on salt-alkali lands and the restoration of vegetation in such areas. This study utilized salt-alkali tolerance Medicago sativa 'Zhaodong' (ZD) and salt-alkali sensitive variety M. sativa 'Zhongmu No.1′ (ZM) as materials. Physiological analyses, transcriptomic sequencing, and hormone-targeted metabolomics techniques were employed to investigate the differential responses of the two alfalfa varieties to NaHCO3 stress in terms of morphology, photosynthetic functionality, and oxidative damage indicators. Additionally, weighted gene co-expression network analysis (WGCNA) was utilized to elucidate key mechanisms underlying salt-alkali tolerance in alfalfa. The results indicate that NaHCO3 stress leads to photosynthetic inhibition and oxidative damage in alfalfa leaves. Under NaHCO3 stress, PSI in alfalfa leaves exhibits higher stability compared to PSII. The salt-alkali tolerance alfalfa variety ZD demonstrates stronger tolerance compared to the salt-alkali sensitive variety ZM. Furthermore, differentially expressed genes (DEGs) between the two varieties under NaHCO3 stress are primarily enriched in KEGG pathways such as chlorophyll synthesis, photosynthesis, carbon fixation, and plant hormone synthesis and signaling. Weighted gene co-expression network analysis (WGCNA) was conducted based on physiological and transcriptomic data. Most differentially expressed genes (DEGs) in the top two modules with the highest correlation to physiological indicators such as photosynthesis are enriched in hormone synthesis and signal transduction pathways. Additionally, key transcription factors involved in hormone signal transduction were identified within these modules, such as MYC2 and ABI5, which regulate jasmonic acid (JA) and abscisic acid (ABA) signaling, respectively. These findings suggest that plant hormone signaling may play a critical role in regulating salt-alkali tolerance in alfalfa. Further analysis was conducted on plant hormone levels and gene expression involved in biosynthesis and signal transduction processes. The results indicate that NaHCO3 stress leads to significant accumulation of ABA and JA content in alfalfa leaves. The biosynthesis and signal transduction pathways of ABA and JA are activated under NaHCO3 stress. Additionally, the salt-alkali tolerance alfalfa variety ZD exhibits a more sensitive response to ABA and JA signals compared to ZM. Salicylic acid (SA) shows a positive response to NaHCO3 stress only in the ZD variety, which may be one of the key reasons for its stronger salt-alkali tolerance. Under NaHCO3 stress, overall growth-promoting hormones (IAA, GA, CK) are downregulated in ZD but upregulated in ZM, indicating that the salt-alkali tolerance alfalfa variety ZD mainly regulates the balance between growth and resistance by modulating the ratio of growth-promoting and stress-related hormones in response to NaHCO3 stress. This study reveals that hormone signaling plays a key role in regulating the photosynthetic function of alfalfa in response to salt-alkali stress, which provides theoretical basis and clues for the molecular breeding of alfalfa for salt-alkali tolerance.

Cyanobacterial Blooms in City Parks: A Case Study Using Zebrafish Embryos for Toxicity Characterization

Cyanobacteria are photosynthetic prokaryotes that play an important role in the ecology of aquatic ecosystems. However, they can also produce toxins with negative effects on aquatic organisms, wildlife, livestock, domestic animals, and humans. With the increasing global temperatures, urban parks, renowned for their multifaceted contributions to society, have been largely affected by blooms of toxic cyanobacteria. In this work, the toxicity of two different stages of development of a cyanobacterial bloom from a city park was assessed, evaluating mortality, hatching, development, locomotion (total distance, slow and rapid movements, and path angles) and biochemical parameters (oxidative stress, neurological damage, and tissue damage indicators) in zebrafish embryos/larvae (Danio rerio). Results showed significant effects for the samples with more time of evolution at the developmental level (early hatching for low concentrations (144.90 mg/L), delayed hatching for high concentrations (significant values above 325.90 mg/L), and delayed development at all concentrations), behavioral level (hypoactivity), and biochemical level (cholinesterase (ChE)) activity reduction and interference with the oxidative stress system for both stages of evolution). This work highlights the toxic potential of cyanobacterial blooms in urban environments. In a climate change context where a higher frequency of cyanobacterial proliferation is expected, this topic should be properly addressed by competent entities to avoid deleterious effects on the biodiversity of urban parks and poisoning events of wildlife, pets and people.

Cells Total Antioxidant Capacity (TAC) and External Expression of Enzymatic Browning for the Commercially Important Penaeids Prawns Parapenaeus longirostris and Penaeus kerathurus

The enzymatic browning process, known also as melanosis, is a significant indicator of oxidative damage in commercially important shrimps and prawns. Total Antioxidant Capacity (TAC) serves as a vital measure of molecular defense against melanosis, a crucial mechanism for organisms to combat detrimental factors such as free radicals. This contribution delves into the assessment of this process for the penaeid species, Parapenaeus longirostris and Penaeus kerathurus. Samples were stored at refrigerator temperature (4 °C) for 0, 1, 2, 4, and 8 days for P. longirostris, and for 0, 2, 4, 8, and 16 days for P. kerathurus. Each day’s samples consisted of groups of ten individuals (5 males, and 5 females). TAC was determined using the CrO5 method. Results revealed an initial TAC increase followed by a gradual decrease over time. Additionally, exterior changes in both species were visually documented daily to capture the macroscopic manifestation of enzymatic browning, aligning with the molecular profile of the samples. Furthermore, Quality Index Method was conducted, where five evaluators graded the organoleptic qualities (texture, odor, color) of the prawn individuals, daily. This assessment aimed to scrutinize the external alterations of the shrimps under refrigeration conditions, revealing changes via sensory evaluation and the Quality Index Method.

Botánica aplicada: radiación UV-B para la obtención de brotes de quinua enriquecidos en compuestos fenólicos, con probables usos en protectores solares naturales o como alimentos funcionales

The objective was to evaluate the use of a microgreen system and very short UV-B radiation dose to obtain plant biomass as a source for phenol-enriched extracts with probable cosmetic and/or food uses. Quinoa seedlings, a native species of the Andes, of two different ages were used. The seedlings were irradiated with different doses of UV-B and then evaluated by quantifying indicators of oxidative damage. Also, the contents of phenolic compounds, photosynthetic pigments, antioxidant capacity, and sun protection factor were determined. The results showed that the youngest seedlings responded better to short UVB doses, increasing the content of soluble and insoluble phenols, without showing oxidative damage. These results were correlated with the greater antioxidant power of the extracts and an intermediate sun protection factor. We conclude that this species, grown in a microgreen system, is a promising alternative to obtain phenol-enriched extracts with possible use in formulations of natural sunscreens. In this sense, these results can serve as a starting point for optimization studies through the response surface methodology.

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.

Screening of differentially expressed RNAs and identifying a ceRNA axis during cadmium-induced oxidative damage in pancreatic β cells

Cadmium, a common metal pollutant, has been demonstrated to induce type 2 diabetes by disrupting pancreatic β cells function. In this study, transcriptome microarray was utilized to identify differential gene expression in oxidative damage to pancreatic β cells following cadmium exposure. The results indicated that a series of mRNAs, LncRNAs, and miRNAs were altered. Of the differentially expressed miRNAs, miR-29a-3p exhibited the most pronounced alteration, with an 11.62-fold increase relative to the control group. Following this, the target gene of miR-29a-3p was identified as Col3a1 through three databases (miRDB, miRTarbase and Tarbase), which demonstrated a decrease across the transcriptome microarray. The upstream target gene of miR-29a-3p was identified as NONMMUT036805, with decreased expression observed in the microarray. Finally, the expression trend of NONMMUT036805/miR-29a-3p/Col3a1 was reversed following NAC pretreatment. This was accompanied by a reduction in oxidative damage indicators, MDA/ROS/GSH-Px appeared to be negatively affected to varying degrees. In conclusion, this study has demonstrated that multiple RNAs are altered during cadmium exposure-induced oxidative damage in pancreatic β cells. The NONMMUT036805/miR-29a-3p/Col3a1 axis has been shown to be involved in this process, which provides a foundation for the identification of potential targets for cadmium toxicity intervention.

Sub-Chronic Methomyl Exposure Induces Oxidative Stress and Inflammatory Responses in Zebrafish with Higher Female Susceptibility.

The widespread use of carbamate pesticides has raised significant environmental and health concerns, particularly regarding water contamination and the disruption of defense systems in organisms. Despite these concerns, research on the differential impacts of pesticides on male and female organisms remains limited. This study focused on methomyl, investigating sex-specific differences in liver antioxidant defenses and inflammatory response indices in male and female zebrafish after 56 days of exposure to environmentally relevant concentrations (0, 0.05, 0.10, and 0.20 mg/L). Our findings indicate that methomyl exposure significantly increased ROS content in zebrafish livers, inducing oxidative stress and activating enzymatic antioxidant defenses such as SOD, CAT, and GSH-Px activities. Sub-chronic exposure altered the expression of apoptosis-related genes (Bax/Bcl2a and Caspases3a), resulting in liver cell apoptosis in a concentration-dependent manner, with the 0.20 mg/L concentration causing the most severe damage. Additionally, methomyl exposure at environmentally relevant concentrations triggered persistent inflammatory responses in liver tissues, evidenced by increased transcription levels of inflammatory factor genes and the activation of toll-like receptors, heightening susceptibility to exogenous allergens. It is noteworthy that oxidative damage indicators (AST, ROS, MDA) and inflammatory gene expressions (IL-1β, TNF-α) were significantly higher in female livers compared to male livers at 0.10-0.20 mg/L methomyl exposure. Consequently, our study underscores the potential adverse effects of environmental methomyl exposure on aquatic organisms and highlights the need for heightened consideration of the risks posed by environmental endocrine disruptors to female health and safety.

Momordin Ic ameliorates psoriasis skin damage in mice via the IL-23/IL-17 axis.

Psoriasis, a chronic and easily recurring inflammatory skin disease, causes a great economic burden to the patient's family because the etiology and mechanism are still unclear and the treatment cycle is long. In this study, the function and related mechanisms of Momordin Ic in psoriasis were investigated. The IMQ-induced mouse psoriasis model was constructed. The protective effects of different doses of Momordin Ic on psoriasis skin damage in mice were detected by PASI score, HE staining and Ki-67 staining. A psoriasis-like keratinocyte model was established at the cellular level using M5 (IL-17A, IL-22, oncostatin M, IL-1α, and TNF-α) triggered HaCaT. The effects of Momordin Ic upon HaCaT cell biological behavior were examined using MTT and CCK-8 assays. In terms of mechanism, the expression level of each inflammatory factor was assessed using IHC staining and/or ELISA, qRT-PCR, the expression of oxidative stress-related indicators was detected biochemically, and western blot was performed to detect the levels of key proteins of the Wnt signaling and VEGF. As the results shown, at the in vivo level, Momordin Ic significantly alleviated skin damage, reduced PASI score and inhibited hyperproliferation of keratinized cells in psoriasis mice. At the cellular level, Momordin Ic also significantly reversed M5-induced hyperproliferation of HaCaT keratinocytes. In terms of mechanism, Momordin Ic significantly inhibited the IL-23/IL-17 axis, dramatically elevated the levels of intracellular antioxidants including SOD, GSH-Px, and CAT, and significantly down-regulated the levels of the indicator of oxidative damage, malondialdehyde (MDA). In addition, Momordin Ic also significantly inhibited the level of β-catenin, a pivotal protein of the Wnt signaling, C-Myc, a target gene of the Wnt signaling, and VEGF, a critical protein of angiogenesis. Inconclusion, Momordin Ic can be involved in the skin-protective effects of psoriasis by multiple mechanisms, including inhibition of the Wnt signaling pathway and the IL-23/IL-17 axis, and suppression of oxidative damageand VEGF expression. Momordin Ic has been proven to be an underlying therapeutic drug for the treatment of psoriasis.

Serum Erythropoietin and Ischemic-Modified Albumin Levels in Adolescents with Obsessive–Compulsive Disorder

Erythropoietin (EPO) has neuroprotective effects by increasing oxidative stress resistance and stabilizing redox balance. Ischemic-modified albumin (IMA) is a product of protein oxidation, and recent evidence suggests that IMA can be used as an indicator of oxidative damage. This study aimed to investigate serum EPO and IMA levels in obsessive–compulsive disorder (OCD) patients and to investigate the relationship between EPO and IMA levels and clinical variables such as disease duration and disease severity. A total of 68 adolescents (11–18 years old), including 35 OCD patients (18 males/17 females) and 33 healthy controls (14 males/19 females) without comorbid disorders matched for age, gender, and BMI, were included in the study. The enzyme-amplified chemiluminescence technique determined serum EPO levels, and serum IMA levels were determined by the spectrophotometric method. Serum EPO levels were lower in OCD patients compared to healthy controls (p = 0.002; Z = − 3.123), and serum IMA levels (ABSU) were significantly higher in the OCD group (p = 0.005). A significant positive correlation was found between IMA levels and the duration of OCD symptoms (p = 0.015, r = 0.409). The study’s findings contribute to the growing body of evidence implicating inflammatory and oxidative processes in the pathogenesis of OCD. The potential of EPO and IMA levels as diagnostic biomarkers for OCD aligns with the ongoing efforts to identify reliable biological markers for the disorder. The positive correlation of IMA levels with the duration of OCD shows the importance of early detection of oxidative damage.

Ibogaine Induces Cardiotoxic Necrosis in Rats-The Role of Redox Processes.

Ibogaine is an organic indole alkaloid that is used in alternative medicine to combat addiction. Numerous cases of life-threatening complications and sudden deaths associated with ibogaine use have been reported, and it has been hypothesized that the adverse effects are related to ibogaine's tendency to induce cardiac arrhythmias. Considering that the bioavailability of ibogaine and its primary metabolite noribogaine is two to three times higher in female rats than in male rats, we here investigated the effect of a single oral dose (1 or 20 mg/kg) of ibogaine on cardiac histopathology and oxidative/antioxidant balance. Our results show that ibogaine induced dose-dependent cardiotoxic necrosis 6 and 24 h after treatment and that this necrosis was not a consequence of inflammation. In addition, no consistent dose- and time-dependent changes in antioxidant defense or indicators of oxidative damage were observed. The results of this study may contribute to a better understanding of ibogaine-induced cardiotoxicity, which is one of the main side effects of ibogaine use in humans and is often fatal. Nevertheless, based on this experiment, it is not possible to draw a definitive conclusion regarding the role of redox processes or oxidative stress in the occurrence of cardiotoxic necrosis after ibogaine administration.

Rosmarinic acid, a natural polyphenol, has a potential pro-oxidant risk via NADH-mediated oxidative DNA damage

BackgroundRosmarinic acid (RA) has a wide range of beneficial effects on human health. On the other hand, RA has been reported to induce metal-mediated reactive oxygen species (ROS) generation and DNA damage. However, its mechanism remains unknown. In this study, to clarify the underlying mechanism, we analyzed metal-mediated DNA damage in isolated DNA treated with RA and its analog isorinic acid.ResultsRA plus Cu(II), but not Fe(III), significantly increased 8-oxo-7,8-dihydro-2’-deoxyguanosine (8-oxodG) formation, an indicator of oxidative DNA damage, in calf thymus DNA. Furthermore, a comparison of the 8-oxodG formation induced by RA and its analog isorinic acid suggested that the catechol groups in RA could be associated with their abilities to form 8-oxodG. Interestingly, the 8-oxodG formation induced by RA and isorinic acid plus Cu(II) was markedly enhanced by the addition of NADH, an endogenous reductant. To elucidate the mechanism of RA plus Cu(II)-induced oxidative DNA damage, we examined DNA damage in 32P-labeled DNA treated with RA in the presence of Cu(II). RA plus Cu(II) caused DNA cleavage, which was enhanced by piperidine treatment, suggesting that RA causes not only DNA strand breakage but also base modification. RA plus Cu(II)-induced DNA damage was inhibited by catalase (H2O2 scavenger), bathocuproine (Cu(I) chelator), and methional (scavenger of a variety of ROS other than •OH) but not by typical •OH scavengers and SOD, indicating the involvement of H2O2, Cu(I), and ROS other than •OH. DNA cleavage site analysis showing RA-induced site-specific DNA damage (frequently at thymine and some cytosine residues) supports the involvement of ROS other than •OH, because •OH causes DNA cleavage without site specificity. Based on these results, Cu(I) and H2O2 generation with concomitant RA autoxidation could lead to the production of Cu(I)-hydroperoxide, which induces oxidative DNA damage. o-Quinone and o-semiquinone radicals are likely to be again reduced to RA by NADH, which dramatically increases oxidative DNA damage, particularly at low concentrations of RA.ConclusionsIn this study, physiologically relevant concentrations of RA effectively induced oxidative DNA damage in isolated DNA through redox cycle reactions with copper and NADH.

Lipophilic fluorescent products as a potential biomarker of oxidative stress: A link between central (brain) and peripheral (blood).

Oxidative stress plays a key role in brain damage because of the sensitivity of brain tissue to oxidative damage. Biomarkers with easy measurement can be a candidate for reflecting the oxidative stress issue in humans. For this reason, we need to focus on specific metabolic products of the brain. End products of free radical reactions such as malondialdehydes form fluorescent products known as lipophilic fluorescent products (LFPs). The distinctive feature of LFPs is their autofluorescent properties. LFPs are detectable in the brain and cerebrospinal fluid. Furthermore, because of the diffusion into the bloodstream, these lipophilic molecules can be detected in the blood. Accumulations of these compounds produce more reactive oxygen species and increase the sensitivity of cells to oxidative damage. Hence, LFPs can be considered a danger signal for neurons and can be introduced as a strong index of oxidative damage both in the central and in the peripheral.

Short-term anaerobic treatment with microperforated packaging enhanced postharvest quality of Stropharia rugosoannulata mushrooms

This study explored the impact of short-term anaerobic treatment combined with microperforated packaging (SAT-MP) on the postharvest quality and physiology of Stropharia rugosonulata mushrooms at 3 ℃. Results indicated that both SAT-MP treatments (T1, T2) and microperforated packaging alone (T3) establish a favorable environment with low O2 (8%−12%) and high CO2 (around 10%). All treatment groups showed significant improvements in firmness, color, and internal structure. Specifically, T1, T2, and T3 exhibited 38%, 41%, and 24% greater stipe firmness and 119%, 173%, and 48% lower browning index, respectively, compared to the control. These treatments also maintained high levels of antioxidant enzyme activity, including Superoxide Dismutase (SOD), Catalase (CAT), Peroxidase (POD), and Ascorbate Peroxidase (APX), as well as non-enzymatic antioxidants such as total phenols, flavonoids, and ascorbic acid. The combined treatment demonstrated the most significant effect, activating the mushroom's antioxidant system, reducing malondialdehyde (MDA) content, conductivity, and ethanol/acetaldehyde accumulation, thus mitigating lipid peroxidation. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) results confirmed better preservation of tissue and cell structure with the 12 h anaerobic treatment. Correlation analysis showed a negative correlation between firmness and oxidative damage indicators, as well as with the browning index and antioxidant-related indicators. Overall, short-term anaerobic treatment with microperforated packaging enhanced antioxidant capacity, maintains reactive oxygen species (ROS) metabolism balance, and cell membrane integrity, effectively delaying firmness decline and browning, highlighting its critical role in extending shelf life.

Comparison of the Antioxidant Potency of Four Triterpenes of Centella asiatica against Oxidative Stress.

We comparatively evaluated the antioxidant properties of key triterpenes from Centella asiatica, including asiatic acid (AA), asiaticoside, madecassic acid, and madecassoside, in several cell types, including skin fibroblasts, macrophages, hepatocytes, and endothelial cells, under conditions promoting oxidative stress. AA conferred the highest viability on Hs68 cells exposed to ultraviolet B (UVB) irradiation. Triterpene pretreatment attenuated the UVB-induced generation of reactive oxygen species (ROS) and malondialdehyde (MDA), as well as the UVB-induced depletion of glutathione (GSH) in skin fibroblasts. AA most potently inhibited UVB-induced MMP generation, resulting in increased intracellular collagen levels. Pretreatment with triterpenes, particularly AA, significantly improved cell viability and attenuated TBHP-induced levels of ROS, alanine aminotransferase, and aspartate aminotransferase in HepG2 cells. Triterpenes attenuated ROS levels and reduced MDA and GSH expression in EA.hy926 cells. In RAW264.7 macrophages, production of nitric oxide, tumor necrosis factor-α, and interleukin-6 (indicators of LPS-induced oxidative damage) was significantly reduced by treatment with any of the triterpenes. Statistical analyses of triterpene biological activities using principal component analysis and hierarchical clustering revealed that AA exerted the greatest overall influence and showed remarkable activity in Hs68 and HepG2 cells.

Protective Effect of Resveratrol Combined with Levodopa Against Oxidative Damage in Dopaminergic Neurons.

Levodopa (L-3,4-dihydroxyphenylalanine, L-Dopa) alleviates the symptoms of Parkinson's disease (PD), yet prolonged usage may give rise to severe adverse effects. Resveratrol (RSV) is a potent antioxidant, anticancer and anti-inflammatory agent. And a variety of polyphenol antioxidant compounds derived from RSV combined with levodopa have demonstrated neuroprotective activity against neuronal cell death. The purpose of this study was to examine the impact of this combination of RSV and L-Dopa on the survival rate, growth status, and reactive oxygen species (ROS) of MES23.5 dopamine (DA) neuron cells. In this study, we induced MPP+ in MES23.5 dopamine neuron cells and observed their survival rate, growth status, ROS content, as well as the effect of RSV combined with L-Dopa on cell survival. We also measured malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity levels as indicators of mitochondrial function, oxidative stress, and oxidative damage in the cells. Our results indicated that the MES23.5 dopamine neurons had decreased survival, poor growth status, and increased ROS content after MPP+ induction. Moreover, we found that MDA levels were elevated, and SOD activity levels were decreased, suggesting that the cells experienced abnormal mitochondrial function. However, when RSV was combined with L-Dopa, the cells showed a reduced level of MPP + -induced oxidative damage, with a more significant inhibitory effect observed in the RSV group at a concentration of 50 μmol/L. In conclusion, we found that the effects of co-administration of RSV with L-Dopa (100 μmol/L) was more effective than L-Dopa administered at the high dose. Thus, we found that RSV has the potential to reduce the dose of L-Dopa required to improve PD symptoms.

Protective Effect of Prunella vulgaris L. Whole Plant or Spicas Water Extracts on Hyperthyroidism with Liver-yang Hyperactivity Syndrome

Background: Prunella vulgaris L. (Lamiaceae) is a perennial medicinal plant commonly used to treat thyroid dysfunction, infectious hepatitis, and mastitis in north-east Asia and Europe. In China, there has been a historical change in the medicinal use of P. vulgaris from the use of whole plants to the use of the spicas. Purpose: This study aimed to evaluate the protective effects of whole plant P. vulgaris water extracts and spicas on hyperthyroidism with liver-yang hyperactivity syndrome and to preliminarily explain the mechanism of action of these water extracts. Methods: Rats were induced with aconite decoction and levothyroxine and treated with P. vulgaris whole plant and spicas water extract for 28 days at the same time. Body weight, food intake, and rectal temperature were monitored. The serum thyroid function indicators thyroid stimulating hormone (TSH), thyroid hormone-free triiodothyronine (FT3) and free thyroxine (FT4), liver function index alanine aminotransferase (ALT) and aspartate aminotransferase (AST), oxidative damage index malondialdehyde (MDA), and superoxide dismutase (SOD) were detected. Liver and thyroid tissues were taken for sectioning and observation. The liver inflammatory factors human tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were detected by immunohistochemistry, and the expression levels of the apoptotic proteins caspase-3 and B-cell lymphoma-2 (Bcl-2) were detected. Results: Both P. vulgaris whole plant and spica water extract groups exhibited markedly reduced FT3 and FT4 contents, increased the TSH content, and decreased ALT and AST activities. Furthermore, these agents improve thyroid and liver lesion tissue; reduce MDA content; increase SOD activity; reduce IL-6, TNF-α, and caspase-3 expression; and increase Bcl-2 expression. Conclusion: The whole plant and spicas water extracts of P. vulgaris have obvious protective effects on hyperthyroidism and hyperactivity in liver yang, and the protective effect of the water extract of spicas is greater than that of the whole plant water extract.

Dietary copper improves intestinal structural integrity in juvenile grass carp (Ctenopharyngodon idella) probably related to its increased intestinal antioxidant capacity and apical junction complex

This research evaluated the effects of copper (Cu) on intestinal antioxidant capacity and apical junctional complex (AJC) in juvenile grass carp. A total of 1080 healthy juvenile grass carp (11.16 ± 0.01 g) were fed six diets including different dosages of Cu, namely 0, 2, 4, 6, 8 mg/kg (Cu citrate [CuCit] as Cu source) and 3 mg/kg (CuSO4·5H2O as Cu source). The trial lasted for 9 weeks. The findings revealed that dietary optimal Cu supplementation (2.2 to 4.1 mg/kg) promoted intestinal growth, including intestinal length, intestinal length index, intestinal weight, and intestinal somatic index (P < 0.05). Furthermore, optimal Cu boosted the intestinal mucosal barrier in juvenile grass carp. On the one hand, optimal Cu reduced diamine oxidase and D-lactate levels in serum (P < 0.05), reduced levels of the oxidative damage indicators malondialdehyde, reactive oxygen species (ROS), protein carbonyl, superoxide dismutase (P < 0.05), and catalase mRNA levels were elevated (P < 0.05), thus boosting intestinal antioxidant capacity, the binding protein Keap1a/1b/Nrf2 signaling pathway might be involved. Optimal Cu had no impact on glutathione peroxidase 1b (GPx1b) gene expression (P > 0.05). On the other hand, optimal Cu increased intestinal tight junction (TJ) proteins (except for claudin 15b) and adherens junction (AJ) proteins (E-cadherin, α-catenin, β-catenin, nectin and afadin) mRNA levels (P < 0.05), which could be connected to the signaling pathway formed by the Ras homolog gene family, member A (RhoA), Rho-associated kinase (ROCK), and myosin light chain kinase (MLCK). Finally, based on serum indicator D-lactate and intestinal oxidative damage index (ROS), Cu requirement (CuCit as Cu source) for juvenile grass carp from initial weight to final weight (from 11 to 173 g) was determined to be 4.14 and 4.12 mg/kg diet, respectively. This work may provide a theoretical foundation for identifying putative Cu regulation pathways on fish intestinal health.

Investigation of oxidative stress profile and pathomorphology of lungs in goats sick of pneumonia-enteritis complex

Peste des Petits Ruminants (PPR), which causes pneumonia-enteritis complex, is an acute, highly contagious disease causing immunosuppression and high mortality in sheep and goats. Epidemiology, clinical signs and pathologic findings of the disease have been studied, but information on the oxidative stress profile is scanty. This study investigated the oxidative stress profile and the pulmonary histopathology of PPR infected goats. Twenty male goats were used for this study. The unvaccinated goats were naturally exposed to PPR according to environmental and animal market conditions consistent with routine PPR virus exposure in endemic areas. Following confirmation of PPR in the goats, their blood and serum samples were collected and evaluated for biomarkers of oxidative stress such as superoxide dismutase, malondialdehyde and catalase, while the neutrophil: lymphocyte ratio (NLR) and serum electrolytes were used to assess physiologic stress. Four goats were euthanized before onset of the clinical signs and every three days following clinical manifestations. Severity of histopathology observed in the lungs were scored and used to categorize the goats into four groups as; normal, mild, moderate and severe. Results showed that oxidative stress increased in PPR affected goats from moderate and severe pulmonary lesions as the disease progressed. On the basis of pulmonary histopathology, malondialdehyde was a better indicator of oxidative damage than superoxide dismutase and catalase. The study also indicated that NLR and Ca:P are reliable indicators of generalised physiologic stress in goats naturally affected by PPR

In vivo chronic exposure to inorganic mercury worsens hypercholesterolemia, oxidative stress and atherosclerosis in the LDL receptor knockout mice

Heavy metal exposure leads to multiple system dysfunctions. The mechanisms are likely multifactorial and involve inflammation and oxidative stress. The aim of this study was to evaluate markers and risk factors for atherosclerosis in the LDL receptor knockout mouse model chronically exposed to inorganic mercury (Hg) in the drinking water. Results revealed that Hg exposed mice present increased plasma levels of cholesterol, without alterations in glucose. As a major source and target of oxidants, we evaluated mitochondrial function. We found that liver mitochondria from Hg treated mice show worse respiratory control, lower oxidative phosphorylation efficiency and increased H2O2 release. In addition, Hg induced mitochondrial membrane permeability transition. Erythrocytes from Hg treated mice showed a 50% reduction in their ability to take up oxygen, lower levels of reduced glutathione (GSH) and of antioxidant enzymes (SOD, catalase and GPx). The Hg treatment disturbed immune system cells counting and function. While lymphocytes were reduced, monocytes, eosinophils and neutrophils were increased. Peritoneal macrophages from Hg treated mice showed increased phagocytic activity. Hg exposed mice tissues present metal impregnation and parenchymal architecture alterations. In agreement, increased systemic markers of liver and kidney dysfunction were observed. Plasma, liver and kidney oxidative damage indicators (MDA and carbonyl) were increased while GSH and thiol groups were diminished by Hg exposure. Importantly, atherosclerotic lesion size in the aorta root of Hg exposed mice were larger than in controls. In conclusion, in vivo chronic exposure to Hg worsens the hypercholesterolemia, impairs mitochondrial bioenergetics and redox function, alters immune cells profile and function, causes several tissues oxidative damage and accelerates atherosclerosis development.

Significant Increase in Oxidative Stress Indices in Erythrocyte Membranes of Obese Patients with Metabolically-Associated Fatty Liver Disease.

Metabolic dysfunction-associated hepatic steatosis (MAFLD) indicates the metabolic risk associated with hepatic steatosis, overweight and obesity, and clinical evidence of metabolic dysregulation. Since MAFLD is one of the diseases that show a high frequency of alterations in the lipid content of cell membranes, the aim of this study was to evaluate the indices of oxidative damage of erythrocyte membranes in overweight and obese MAFLD subjects. The study was conducted on serum samples and red blood cell membranes of overweight and obese MAFLD subjects. For each patient, biochemical measurements and lipidomic analyses of erythrocytes membranes were performed. Significant differences in fatty acid profiles of RBC membranes were found between overweight and obese patients. In particular, the Peroxidation Index (PI) was higher in the erythrocyte membranes of obese subjects than in overweight subjects. The same behavior was observed for Unsaturation Index (UI) and Free Radical Stress Index (Free RSI), supporting the fact that the systemic increase in oxidative stress was associated with obesity. The study shows that there is a different susceptibility to erythrocyte membrane peroxidation for overweight and obese subjects, and the increased values of oxidative stress indices observed in the erythrocyte membranes of obese patients with MAFLD may be a possible indicator of pro-oxidative events occurring in obesity-related diseases.