Indicator Of Oxidative Damage Research Articles

On the mechanisms of cardiotoxic action of various nanoparticles in experimental studies in vivo and in vitro

Nanoparticles are the main product of artificial technologies, and also accompany production processes in various industries. The main routes of exposure to nanoparticles are through the respiratory tract, skin and orally; therefore, most toxicological studies have focused on the lungs, liver and skin. Nanoscale particles easily penetrate the alveolar-capillary barrier and enter the bloodstream of the body. Thus, they can reach various organs, accumulate, cause toxicity, and the heart is one of the target organs.
 The study aims to search and systematize the literature data on the mechanisms of cardiotoxic action of nanoparticles of various chemical nature (elemental, elementoxide).
 The researchers conducted a literature review as part of a study of the cardiotoxic effect of nanoparticles on the body. The review is based on modern original research. When searching for literary sources, the authors used the following information databases: PubMed, Google Scholar, CyberLeninka Scientific Electronic Library, Russian Scientific Electronic Library eLibrary.Ru. In total, there were 37 original articles in the review, including 35 foreign ones, and 15 — no older than 5 years. The development of oxidative stress and an inflammatory reaction leads to the formation of cardiotoxicity of nanomaterials, which subsequently leads to necrosis and apoptosis of cells.
 Indicators of oxidative damage to lipids and DNA molecules indicate that the tissues of the heart and lungs suffer from oxidative stress not only as a result of an increase in the formation of reactive oxygen species, but also due to a malfunction of antioxidant mechanisms caused by exposure to nanoparticles.
 Studies using endothelial cells have shown that exposure to metal and metal oxide nanoparticles can promote the release of cytokines, the expression of adhesion molecules and monocyte adhesion, which are key events associated with the development of cardiovascular diseases.
 These results, combined with other in vitro data, suggest that direct contact of the cardiovascular system with metal-based nanoparticles may cause cardiovascular toxicity associated with inflammatory reactions, oxidative stress, autophagy dysfunction and endoplasmic reticulum stress. Oxidative stress induced by nanoparticles leads to apoptosis and inflammatory reactions in cardiomyocytes, as well as disrupts the integrity of mitochondrial membranes and cell organelles, leading to various heart pathologies. One of the main mechanisms of toxicity of nanoparticles of different chemical nature is oxidative stress.

Effect of intermittent fasting on adriamycin-induced nephropathy: Possible underlying mechanisms

PurposeIntermittent fasting (IF) has been shown to induce a well-organized adaptive defense against stress inside the cells, which increases the production of anti-oxidant defenses, repair of DNA, biogenesis of mitochondria, and genes that combat inflammation. So, the goal of the current investigation was to identify the effects of IF on rats with adriamycin (ADR)-induced nephropathy and any potential underlying mechanisms. MethodsFour groups of 40 mature Sprague-Dawley male rats were allocated as follow; control, fasting, ADR, and ADR plus fasting. After 8 weeks of ADR administration urine, blood samples and kidneys were taken for assessment of serum creatinine (Cr), BUN, urinary proteins, indicators of oxidative damage (malondialdehyde (MDA), reduced glutathione (GSH) and Catalase (CAT) levels), histopathological examinations, immunohistochemical examinations for caspase-3, Sirt1, aquaporin2 (AQP2) and real time PCR for antioxidant genes; Nrf2, HO-1 in kidney tissues. ResultsIF significantly improved serum creatinine, BUN and urinary protein excretion, oxidative stress (low MDA with high CAT and GSH), in addition to morphological damage to the renal tubules and glomeruli as well as caspase-3 production during apoptosis. Moreover, IF stimulates significantly the expression of Sirt1 and Nrf2/HO-1 and AQP2. ConclusionAQP2, Sirt1, Nrf2/HO-1 signaling may be upregulated and activated by IF, which alleviates ADR nephropathy. Enhancing endogenous antioxidants, reducing apoptosis and tubulointerstitial damage, and maintaining the glomerular membrane's integrity are other goals.

How Does Altering the Volume-Load of Plyometric Exercises Affect the Inflammatory Response, Oxidative Stress, and Muscle Damage in Male Soccer Players?

Incorporating plyometric exercises (PE) into soccer players' conditioning routines is vital for boosting their performance. Nevertheless, the effects of PE sessions with diverse volume loads on inflammation, oxidative stress, and muscle damage are not yet clearly understood. This study aimed to examine the effects of altering the volume-loads of PE on indicators of oxidative muscle damage and inflammation. The study involved forty young male soccer players who were randomly assigned to three different volume-loads of PE (Low volume-load [100 jumps]: LVL, n = 10; Moderate volume-load [150 jumps]: MVL, n = 10; and High volume-load [200 jumps]: HVL, n = 10) and a control group (CON = 10). The levels of various biomarkers including delayed onset muscle soreness (DOMS), serum lactate dehydrogenase (LDH), creatine kinase (CK), 8-hydroxy-2-deoxyguanosine (8-OHdG), malondialdehyde (MDA), protein carbonyl (PC), leukocytes, neutrophils, interleukin-6 (IL-6), and C-reactive protein (CRP) were measured at different time points. These measurements were taken at rest, immediately after completion of PE, and 24-, 48-, and 72-hours post-PE. The CK, LDH, DOMS, 8-OHdG, MDA, and PC levels were significantly increased (p < 0.05) after the PE protocol, reaching their peak values between 24 to 48 hours post-PE for all the volume-loaded groups. The levels of leukocytes, neutrophils, and IL-6 also increased after the PE session but returned to resting values within 24 hours post-PE. On the other hand, CRP levels increased at 24 hours post-PE for all the treatment groups (p < 0.05). The changes observed in the indicators of muscle damage and inflammation in response to different volume-loads of PE was not significant. However, the HVL and MVL indicated significant differences compared to LVL in the 8-OHdG (at 48-hour) and MDA (at 72-hour). Athletes engaging in higher volume-loads demonstrated more pronounced responses in terms of biochemical variables (specifically, LVL < MVL < HVL); however, these changes were not statistically significant (except 8-OHdG and MDA).

Effect of PERLA®, a new cold-storage solution, on oxidative stress injury and early graft function in rat kidney transplantation model

BackgroundThe composition of organ preservation solutions is crucial for maintaining graft integrity and early graft function after transplantation. The aim of this study is to compare new organ preservation solution PERLA® with the gold standard preservation solution University of Wisconsin (UW) regarding oxidative stress and early graft injury.MethodsIn order to assess oxidative stress after cold storage, kidney grafts have been preserved for 18 h at 4° C in either UW solution or PERLA® solution and then assessed for oxidative stress injury (protocol 1). To assess kidney injuries and oxidative stress after reperfusion, rat kidneys were harvested, stored in cold UW or in PERLA® solutions for 18 h at 4 °C and then transplanted heterotopically for 6 h (protocol 2). PERLA® is a high Na+/low K+ solution including PEG-35 (1 g/L), trimetazidine (1 µM), carvedilol (10 µM) and tacrolimus (5 µM).ResultsOur results showed that preservation of kidneys in PERLA® solution significantly attenuates oxidative stress parameters after cold storage and reperfusion. We found a significant decrease in oxidative damage indicators (MDA, CD and CP) and a significant increase in antioxidant indicators (GPx, GSH, CAT, SOD and PSH). Moreover, PERLA® solution decreased kidney injury after reperfusion (creatinine, LDH and uric acid).ConclusionPERLA® solution was more effective than UW storage solution in preserving rat’s kidney grafts.

The Effect of Vacuuming on the Storage Stability of Canned Meat in Retort Bags

The article presents the results of a study of the quality of ‘Beef Stew’ canned meat packaged in retort bags in the usual way and under vacuum. It was found that when stored in warehouse conditions during the shelf life (24 months), canned food in terms of safety and quality met the requirements of the TR CU and the standard. The indicators of oxidative damage were within the experimentally established critical values. According to the data obtained, with the same shelf life, canned meat packed in retort bags with vacuuming retains consumer properties better than canned food without vacuum.

Physiological changes in captive elephants in northern Thailand as a result of the COVID-19 tourism ban-stress biomarkers.

The international travel ban instituted by the Thai government in March 2020 in response to the COVID-19 pandemic greatly affected how tourist camp elephants were managed, with reductions in exercise opportunities, longer chaining hours, and diminished food provisioning. This study was conducted to determine how those changes affected health and welfare biomarkers in individual elephants over the 2 years of the countrywide lockdown (April 2020-April 2022). Blood and fecal samples were collected from 58 elephants at six camps (monthly in Year 1, quarterly in Year 2) and analyzed for stress biomarkers - fecal glucocorticoid metabolites (fGCM), serum oxidative stress [malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG)], and stress leukograms. Overall, fGCM concentrations increased within the first few months and remained higher than pre-COVID levels, as did the H/L ratio, a measure affected by cortisol. Serum 8-OHdG, an indicator of DNA oxidative damage, also increased over time, while monocytosis and lymphopenia further suggested alterations in immune function as a result of stress. By contrast, another marker of oxidative stress, serum MDA, declined, possibly in response to reduced roughage and supplement intake. A notable finding was a seasonal pattern of fGCM that was significantly different from previous studies. Whereas higher fGCM during the rainy season were observed in this study, previously, concentrations were highest during the winter, high tourist season. Thus, ironically, both the presence and absence of tourists have been associated with increased fGCM concentrations, albeit for different reasons. Camp management factors negatively affecting stress outcomes included shorter chain lengths, longer chain hours, lack of exercise, and reduced roughage and supplements. Overall, it was clear that camps struggled to maintain adequate care for elephants during the COVID-19 pandemic, highlighting the importance of tourist income and need for contingency plans to cope with potential future disruptions to tourism.

Effects of exogenous GABA on physiological characteristics of licorice seedlings under saline-alkali stress

Licorice is widespread in arid and semi-arid areas, but high soil salinity has always been a limiting factor for vegetation growth in these areas. Gamma-aminobutyric acid (GABA) is a signaling molecule that can regulate tolerance in plant. However, the mechanism by which exogenous GABA regulates the response of licorice to saline-alkali stress is not yet clear. In this study, we investigated the effects of exogenous GABA on growth parameters, oxidative damage, hormone levels and photosynthetic indices of licorice seedlings under different combinations of saline and alkali stress conditions. The experiment involved eight treatments: CK, distilled water (control); CK + GABA, 0.1 mM GABA; salt stress (SS), 150 mM NaCl; SS + GABA, 150 mM NaCl + 0.1 mM GABA; alkali stress (AS), 10 mM Na2CO3; AS + GABA, 10 mM Na2CO3 + 0.1 mM GABA; mixed saline-alkali stress (MAS), 150 mM NaCl + 10 mM Na2CO3; MAS + GABA, 150 mM NaCl + 10 mM Na2CO3 + 0.1 mM GABA. Our results showed that the inhibitory effects of SS and MAS on the seedling height, root length and root-shoot ratio were significantly alleviated by exogenous GABA. Although soluble sugars, chlorophyll a, total chlorophyll, and superoxide dismutase (SOD) activity were lower in the leaves of the seedlings in the SS treatment compared with the control, these physiological parameters increased significantly after GABA application. Exogenous GABA improved glutathione (GSH) activity in both the leaves and roots of the seedlings during the AS treatment. Additionally, take advantage of GABA led to an increase in ABA, GA and IAA contents in leaves under SS, AS and MAS treatments. Furthermore, the photosynthetic parameters, including Pn, gs, Tr, ETR and qP, significantly increased following the utilization of GABA in both the SS and MAS treatments. Therefore, the application of exogenous GABA can reduce the accumulation of harmful substances, preserve cell morphology, and enhance cell function under saline, alkali, and saline-alkali stress. This enhances the resistance of licorice seedlings to stress conditions and reduces physiological damage.

Bacillus velezensis A2 Can Protect against Damage to IPEC-J2 Cells Induced by Zearalenone via the Wnt/FRZB/β-Catenin Signaling Pathway.

Zearalenone (ZEA) has adverse effects on human and animal health, and finding effective strategies to combat its toxicity is essential. The probiotic Bacillus velezensis A2 shows various beneficial physiological functions, including the potential to combat fungal toxins. However, the detailed mechanism by which the Bacillus velezensis A2 strain achieves this protective effect is not yet fully revealed. This experiment was based on transcriptome data to study the protective mechanism of Bacillus velezensis A2 against ZEA-induced damage to IPEC-J2 cells. The experiment was divided into CON, A2, ZEA, and A2+ZEA groups. This research used an oxidation kit to measure oxidative damage indicators, the terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) method to detect cell apoptosis, flow cytometry to determine the cell cycle, and transcriptome sequencing to screen and identify differentially expressed genes. In addition, gene ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were adopted to screen out relevant signaling pathways. Finally, to determine whether A2 can alleviate the damage caused by ZEA to cells, the genes and proteins involved in inflammation, cell apoptosis, cell cycles, and related pathways were validated using a quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot methods. Compared with the CON group, the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) in the ZEA group increased significantly (p < 0.01), while the levels of antioxidant enzyme activity, total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-PX), total antioxidant capacity (T-AOC), and catalase (CAT) decreased significantly (p < 0.01). Compared with the ZEA group, the A2+ZEA group showed a significant decrease in ROS and MDA levels (p < 0.01), while the levels of T-SOD, GSH-PX, T-AOC, and CAT increased significantly (p < 0.01). TUNEL and cell cycle results indicated that compared with the ZEA group, the A2+ZEA group demonstrated a significant decrease in the cell apoptosis rate (p < 0.01), and the cell cycle was restored. Combining transcriptome data, qRT-PCR, and Western blot, the results showed that compared with the CON group, the mRNA and protein expression levels of Wnt10 and β-catenin increased significantly (p < 0.01), while the expression level of FRZB decreased significantly (p < 0.01); compared with the ZEA group, the expression levels of these mRNA and proteins were reversed. Bacillus velezensis A2 can increase the antioxidant level, reduce inflammatory damage, decrease cell apoptosis, and correct the cell cycle when that damage is being caused by ZEA. The protective mechanism may be related to the regulation of the Wnt/FRZB cell/β-catenin signaling pathway.

Elevated tropospheric ozone and crop production: potential negative effects and plant defense mechanisms.

Ozone (O3) levels on Earth are increasing because of anthropogenic activities and natural processes. Ozone enters plants through the leaves, leading to the overgeneration of reactive oxygen species (ROS) in the mesophyll and guard cell walls. ROS can damage chloroplast ultrastructure and block photosynthetic electron transport. Ozone can lead to stomatal closure and alter stomatal conductance, thereby hindering carbon dioxide (CO2) fixation. Ozone-induced leaf chlorosis is common. All of these factors lead to a reduction in photosynthesis under O3 stress. Long-term exposure to high concentrations of O3 disrupts plant physiological processes, including water and nutrient uptake, respiration, and translocation of assimilates and metabolites. As a result, plant growth and reproductive performance are negatively affected. Thus, reduction in crop yield and deterioration of crop quality are the greatest effects of O3 stress on plants. Increased rates of hydrogen peroxide accumulation, lipid peroxidation, and ion leakage are the common indicators of oxidative damage in plants exposed to O3 stress. Ozone disrupts the antioxidant defense system of plants by disturbing enzymatic activity and non-enzymatic antioxidant content. Improving photosynthetic pathways, various physiological processes, antioxidant defense, and phytohormone regulation, which can be achieved through various approaches, have been reported as vital strategies for improving O3 stress tolerance in plants. In plants, O3 stress can be mitigated in several ways. However, improvements in crop management practices, CO2 fertilization, using chemical elicitors, nutrient management, and the selection of tolerant crop varieties have been documented to mitigate O3 stress in different plant species. In this review, the responses of O3-exposed plants are summarized, and different mitigation strategies to decrease O3 stress-induced damage and crop losses are discussed. Further research should be conducted to determine methods to mitigate crop loss, enhance plant antioxidant defenses, modify physiological characteristics, and apply protectants.

Melatonin attenuates liver injury in arsenic-treated rats: The potential role of the Nrf2/HO-1, apoptosis, and miR-34a/Sirt1/autophagy pathways.

Arsenic is a toxic metalloid found in the environment in different organic and inorganic forms. Molecular mechanisms implicated in arsenic hepatotoxicity are complex but include oxidative stress, apoptosis, and autophagy. The current study focused on the potential protective capacity of melatonin against arsenic-induced hepatotoxicity. Thirty-six male Wistar rats were allocated into control, arsenic (15 mg/kg; orally), arsenic (15 mg/kg) plus melatonin (10, 20, and 30 mg/kg; intraperitoneally), and melatonin alone (30 mg/kg) groups for 28 days. After the treatment period, the serum sample was separated to measure liver enzymes (AST and ALT). The liver tissue was removed and then histological alterations, oxidative stress markers, antioxidant capacity, the levels of Nrf2 and HO-1, apoptosis (Bcl-2, survivin, Mcl1, Bax, and caspase-3), and autophagy (Sirt1, Beclin-1, and LC3 II/I ratio) proteins, as well as the expression level of miR-34a, were evaluated on this tissue. Arsenic exposure resulted in the enhancement of serum AST, ALT, and substantial histological damage in the liver. Increased levels of malondialdehyde, a lipid peroxidation marker, and decreased levels of physiological antioxidants including glutathione, superoxide dismutase, and catalase were indicators of arsenic-induced oxidative damage. The levels of Nrf2, HO-1, and antiapoptotic proteins diminished, while proapoptotic and autophagy proteins were elevated in the arsenic group concomitant with a low level of hepatic miR-34a. The co-treatment of melatonin and arsenic reversed the changes caused by arsenic. These findings showed that melatonin reduced the hepatic damage induced by arsenic due to its antioxidant and antiapoptotic properties as well as its regulatory effect on the miR-34a/Sirt1/autophagy pathway.

Human serum albumin-bound paclitaxel nanoparticle inhibits cervical carcinoma cell proliferation and oxidative damage through CYP3A4 and CYP2C8

BackgroundCervical cancer (CC) is currently the most common malignant tumour in the female reproductive tract, and paclitaxel (PTX) is a commonly used chemotherapeutic agent, but tumour cell resistance will seriously affect the therapeutic efficacy of PTX. Nanoparticle human serum albumin-bound paclitaxel (Nano-HSA-PTX) is a novel drug delivery modality that may have superior effects to PTX alone. ObjectiveTo clarify the effect of Nano-HSA-PTX on cervical carcinoma (CC) cells and the underlying mechanisms. MethodsAfter the preparation of Nano-HSA-PTX, its morphology was observed by electron transmission microscope (TEM), and its entrapment efficiency (EE%) and drug loading rate (DL%) were detected. Nano-HSA-PTX was compared with conventional PTX for drug metabolism. Additionally, CC HeLa and SiHa cells were purchased and divided into three groups to treat with Nano-HSA-PTX, PTX and normal saline, respectively. MTT, cell cloning, Transwell and cell scratch assays were carried out to determine cell proliferation, invasion and migration, flow cytometry and Western blotting were performed to detect apoptosis rate and apoptosis-related protein expression, and PCR was conducted to quantify oxidative damage indicators. Further, CYP3A4 and CYP2C8 expression patterns in CC cells (HeLa and SiHa) and human normal cervical epithelia (End1/E6E7) and the changes of their levels under the intervention of Nano-HSA-PTX were measured. Subsequently, C57BL/6mice were purchased for subcutaneous tumorigenesis experiment to observe the impact of Nano-HSA-PTX on tumor growth. ResultsUnder TEM, Nano-HSA-PTX was complete and arranged compactly, with a stable structure and markedly higher EE% and DL% than PTX (P < 0.05). Under Nano-HSA-PTX intervention, the proliferation, invasion, migration and oxidative damage of HeLa and SiHa were significantly decreased compared with the control and PTX groups, while the apoptosis was increased (P < 0.05). Besides, elevated CYP3A4 and CYP2C8 levels were observed in CC cells, which were inhibited by Nano-HSA-PTX and PTX (P < 0.05). Finally, tumorigenesis experiments in nude mice revealed that Nano-HSA-PTX could inhibit tumor growth. ConclusionCompared with PTX, Nano-HSA-PTX has a superior effect of inhibiting CC activity. And this mechanism of action was carried out by inhibiting the expression of CYP3A4 and CYP2C8.

Genetic liability for diet-derived circulating antioxidants, oxidative stress, and risk of osteoarthritis: a Mendelian randomization study.

Although well-documented, the causal relationships between diet-derived circulating antioxidants, oxidative stress, and osteoarthritis (OA) are equivocal. The objective of this study is to employ two-sample Mendelian randomization (MR) to investigate possible causal relationships among dietary-derived circulating antioxidants, oxidative stress damage indicators, and OA risk. Single-nucleotide polymorphisms for diet-derived circulating antioxidants (ascorbate, β-carotene, lycopene, retinol, and α-and γ-tocopherol), assessed as absolute levels and metabolites, as well as oxidative stress injury biomarkers (GSH, GPX, CAT, SOD, albumin, and total bilirubin), were retrieved from the published data and were used as genetic instrumental variables. Summary statistics for gene-OA associations were obtained from publicly available and two relatively large-scale GWAS meta-analyses to date. The inverse-variance weighting method was utilized as the primary MR analysis. Moreover, multivariable MR was used to determine if mediators (BMI and smoking) causally mediated any connection. Furthermore, for each exposure, MR analyses were conducted per outcome database and then meta-analyzed. Genetically predicted absolute retinol level was causally associated with hip OA risk [odds ratios (ORs) = 0.40, 95% confidence interval (CI) = 0.24-0.68, FDR-corrected p = 0.042]. Moreover, genetically predicted albumin level was causally associated with total OA risk (OR = 0.80, 95% CI = 0.75-0.86, FDR-corrected p = 2.20E-11), as well as the risk of hip OA (OR = 0.75, 95% CI = 0.68-0.84, FDR-corrected p = 1.38E-06) and knee OA (OR = 0.82, 95% CI = 0.76-0.89, FDR-corrected p = 4.49E-06). In addition, MVMR confirmed that the effect of albumin on hip OA is independent of smoking initiation, alcoholic drinks per week, and moderate-to-vigorous physical activity levels but may be influenced by BMI. Evidence from our study supports a potentially protective effect of high levels of retinol and albumin on OA risk.

Immune and Oxidative Stress Response of the Fish Xyrichthys novacula Infected with the Trematode Ectoparasite Scaphanocephalus sp. in the Balearic Islands

Global change produces substantial modification to the distribution and rhythm of infection of diseases in fish, favouring the introduction of new pathogens. Recently, the presence of black spot disease, associated with a digenean fluke of the genus Scaphanocephalus, has been observed in specimens of Xyrichthys novacula on the island of Ibiza (Balearic Islands). The aim of the present study was to evaluate the antioxidant and immune response in both the skin mucus and spleen of X. novacula depending on the degree of infection by Scaphanocephalus sp. The specimens were captured in a control area, without the presence of the parasite, and in an affected area, classifying the fish as low infection (1–15 spots) and high infection (&gt;15 spots). As the degree of infection increased, a decrease in the body condition index was observed. The activity of the antioxidant enzymes in the mucus—catalase, superoxide dismutase and glutathione peroxidase—increased progressively with the degree of infection. This activation of antioxidant defences was not enough to prevent an increase in malondialdehyde levels, an indicator of oxidative damage, in the group with the highest infection. Similarly, an increase in immunological parameters—lysozyme, alkaline phosphatase, myeloperoxidase and immunoglobulins—was observed in mucus as infection increased. Regarding the spleen, only an increase in lysozyme activity and alkaline phosphatase in fish with a greater severity of infection was observed. In conclusion, as the severity of Scaphanocephalus sp. infection increased, it induced an immune and oxidative stress response in skin mucus, leading to a decrease in overall body condition. The potential health effects that the ectoparasite may have on X. novacula populations will require follow-up studies.

Effects of sources and routes of administration of vitamins A, D and copper on postnatal status of these micronutrients in piglets.

Twenty-six nulliparous sows were fed conventional gestation and lactation diets supplemented (N = 13) or not (N = 13) with extra daily supplements of 25-hydroxy-cholecalciferol (25-OH-D3; 4 ĸIU), β-carotene (24 ĸIU), and copper (Cu)-proteinate (45 mg) from day 90 of gestation to 21 d of lactation (L21). In each litter, 10 piglets were divided into 5 pairs received, at 2 (L2) and 8 d (L8) of age, one of the five combinations of micronutrient sources and routes of administration (N = 260 piglets total). These neonatal treatments (N = 26 pairs or 52 piglets each) consisted of oral vitamin D3, retinol acetate and CuSO4 (T1); oral 25-OH-D3, β-carotene, and Cu proteinate (T2); exposure to ultraviolet light (UVB), oral retinol palmitate and Cu gluconate (T3); intramuscular vitamin D3 and retinyl propionate and oral Cu acetate (T4); oral saline (CTRL). Oral or intramuscular provisions corresponded to 12 mg of Cu and 70 and 12 ĸIU of vitamins A and D, respectively. Blood samples were collected from all piglets at L2, L8, and L21 for determination of serum Cu, retinol, and 25-OH-D3. Body weight was measured at birth, L2, L8, and L21. Piglets were weaned at L21, and liver and blood samples were collected 2 d later to evaluate oxidative enzymes in blood and liver and hepatic ATP concentrations and expression of genes associated with antioxidant status. Sow treatments had marginal or no impacts on Cu, retinol, 25-OH-D3, or antioxidant status in piglet blood serum and liver. However, when supplements were given to piglets, hepatic Cu was 38% greater in for all treated piglets compared to CTRL (P < 0.01), hepatic retinol was 3 times higher in T1 than in CTRL (P < 0.01) and intermediate for other treatments whereas serum 25-OH-D3 was markedly increased with T2 and T3 at L8 and L21, respectively, compared to CTRL (Piglet treatment × Age interaction, P < 0.01). Concerning antioxidant activities, glutathione peroxidase, and superoxide dismutase were increased (P < 0.03) in plasma of T2 piglets whereas the highest values (P < 0.03) for indicators of oxidative damage to proteins were observed in T4 piglets. The study revealed that oral Cu proteinate from T2, oral retinol acetate from T1, oral 25-hydroxy-cholecalciferol from T2, and UVB light exposure from T3 were the most efficient ways of increasing the postnatal status of these micronutrients in suckling piglets and this may have some impacts on their peri-weaning antioxidant status.

Combined exposure of beta-cypermethrin and emamectin benzoate interferes with the HPO axis through oxidative stress, causing an imbalance of hormone homeostasis in female rats

The impact of pesticides on reproductive health has been increasingly recognized. β-cypermethrin (β-CYP) and emamectin benzoate (EMB) are commonly used with agricultural workers. There are few published studies on the effects of combined poisoning of these two pesticides on the reproductive system. This study investigated the toxic effects and mechanism of β-CYP and EMB on the reproductive system of female rats based on the hypothalamic-pituitary-ovarian (HPO) axis. The hypothalamic GnRH content tended to decrease, and Kiss-1 and GPR-54 mRNA and protein expression tended to increase in exposed rats. FSH content was elevated for the pituitary gland, and Kiss-1 and GPR-54 mRNA and protein expression were enhanced in all experimental groups compared with the control group. E2 content in rat ovaries and ERα mRNA and protein expression were reduced by β-CYP and EMB. Furthermore, there were interactive effects of β-CYP and EMB on FSH and E2 release, pituitary GPR-54 mRNA and protein, and ovarian ERα mRNA expression. To investigate causes of damage, oxidative damage indicators were tested and showed that exposure to β-CYP and EMB decreased GSH-Px and SOD activities in the HPO axis, increased MDA levels in the hypothalamus and ovary together with LDH activities in the HPO axis, with an interaction effect on GSH-Px and SOD activities in the hypothalamus and pituitary gland as well as on MDA in the ovary. The above results support the screening of sensitive molecular biomarkers and evaluation of the adverse effects of pesticide exposure in greenhouse operations on reproductive health.

Ameliorative effects of Dunaliella salina microalgae on nanoparticle (ZnO NPs)-induced toxicity in fish.

Dunaliella salina (D. salina) is a well-known microalga that contains considerable amounts of nutritious and medicinal bioactive components. This work studied the modulatory role of D. salina against zinc oxide nanoparticle (ZnO NPs)-induced neurotoxic effects in adult zebrafish. Fishes were subjected to 0.69mg L-1 (1/5th 96-h LC50) for 4weeks; then, fishes were supplemented with D. salina in the diet for 2weeks at two levels (15 and 30%). Exposure to ZnO NPs induced a significant increase in the levels of reactive oxygen species (ROS), hydrogen peroxide (H2O2), malondialdehyde (MDA), and 8-hydroxy-2-deoxyguanosine (8-OH-dG) while accompanied with downregulation of antioxidant genes in the brain of exposed fishes. Brain neurochemistry and enzyme activities were also altered following ZnO NP exposure. ZnO NPs significantly reduced the neurotransmitters and acetylcholinesterase (AchE) activity while increasing Alzheimer's disease-related proteins and inflammatory response via upregulation of tumor necrosis factor (TNF-α). Additionally, ZnO NPs increased the indices of brain's DNA oxidative damage, increasing brain tissue's metallothionein (MT) and zinc residues. ZnO NPs upregulated the transcription patterns of apoptosis-related genes (casp3 and p53). D. salina dietary co-supplementation with ZnO NPs alleviated the ZnO NPsZnO NP-induced neuro-oxidative damages by lowering the lipid, DNA damage, and inflammatory biomarkers. Besides, D. salina alleviating responses were linked with increasing the levels of the assessed antioxidants. Conclusively, D. salina dietary supplementation induced potential alleviating effects of the ZnO NP-induced neurotoxicity in adult zebrafish.

446 The Effects of Maternal Diet During Gestation on Oxidative Status of Offspring

Abstract Poor maternal nutrition during gestation is common in livestock production and includes both nutrient restriction and over-nutrition. Poor maternal nutrition affects offspring pre- and post-natal growth including decreases in muscularity and increases in adiposity which results in poor quantity and quality of animal products. Oxidative stress, when free radicals exceed the capacity of antioxidants, damages lipid membranes, proteins, and DNA. Oxidative stress may contribute to the poor growth outcomes observed in offspring from poorly nourished dams. Therefore, the objective of this research was to determine the effects of poor maternal nutrition during gestation on offspring circulating oxidative status in sheep. We hypothesized that offspring of restricted- and over-fed ewes would have an altered oxidative status in circulation. To test this hypothesis, multiparous Dorset ewes (n = 45) pregnant with twins were fed 100% (CON), 60% (RES), or 140% (OVER) of National Research Council requirements from d 30 of gestation until parturition. At parturition, ewes were fed a control diet such that the nutritional insult only occurred during gestation. Blood samples were collected from offspring by jugular venipuncture at d 112 and d 224 of age to evaluate oxidative status in circulation. Data were analyzed in SAS 9.4 using PROC MIXED with fixed effects of offspring sex and maternal diet with sampling timepoint as repeated measure. Data were considered significant at P &amp;lt; 0.05. In offspring plasma, superoxide dismutase, an endogenous antioxidant, activity was 17% greater in CON offspring compared with RES and OVER (P ≤ 0.04). Malondialdehyde (MDA), a marker of lipid peroxidation, concentration was not different at d 112 but RES animals had 10% lesser concentration of MDA than CON at d 224 (P ≤ 0.02). Protein carbonyl (PC), a marker of protein oxidation, concentration was 9% greater in CON animals than RES and OVER (P = 0.01). Additionally, PC concentrations were 19% greater at d 224 compared with d 112 (P ≤ 0.001). These results indicate that at the chosen timepoints, RES and OVER offspring had less antioxidant activity but also less indication of oxidative damage. Overall, the alterations in antioxidant activity and oxidative damage suggest dysregulation in circulating oxidative status that may contribute to the negative consequences of poor maternal nutrition during gestation. Future work should focus on the impacts of poor maternal nutrition on oxidative stress in muscle.

Antagonistic effects of N-acetylcysteine on lead-induced apoptosis and oxidative stress in chicken embryo fibroblast cells

Lead (Pb) is a heavy metal that can have harmful effects on the environment, which has severe cytotoxicity in many animal tissues. N-acetylcysteine (NAC) has antioxidant activity, reducing lead-induced oxidative stress and apoptosis, but its role in chicken cells is unknown. The current study explored the antagonistic effect of NAC on lead-induced apoptosis and oxidative stress in chicken embryo fibroblast (CEF). In this study, CEF was used as a model to measure the cytotoxic effects of lead nitrate at different concentrations, demonstrating a dose-dependent effect on CEF activity. Employing inverted microscopy, the investigation of morphological alterations in CEF cells was conducted. Fluorescence staining methodology enabled the assessment of reactive oxygen species (ROS) levels within CEF cells. Moreover, an enzyme-linked immunosorbent assay was utilized to detect the presence of oxidative damage indicators encompassing superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) activity, malondialdehyde (MDA) content, and total antioxidant capacity (T-AOC) within CEF cells. Furthermore, the determination of the apoptosis rate of CEF cells was accomplished through the utilization of the Hoechst 33258 staining method in combination with the Annexin V-FITC dual staining method. By using RT-qPCR for detection, lead treatment increased expression of pro-apoptotic genes, caspase-3, and caspase-9, and reduced expression of anti-apoptotic genes, Bcl-2, and BI-1. Reduced antioxidant capacity was shown by increased ROS and MDA levels in CEF cells after lead treatment. The results showed that NAC inhibited the expression of caspase-3 and caspase-9 in lead-treated CEF cells, while NAC had a certain inhibitory effect on the relative expression of Bcl-2 and BI-1 mRNA in lead-induced CEF cells. NAC significantly reduced lead-induced oxidative damage and apoptosis. Overall, our results demonstrate a novel protective effect of NAC against lead-induced injury in chicken cells, providing a theoretical basis for future investigations of drugs that are effective in preventing lead poisoning in animals.

Relationships between DNA oxidative damage, testosterone, and body mass index in sulfur mustard-chemical veterans

Relationships between DNA oxidative damage, testosterone, and body mass index in sulfur mustard-chemical veterans

Nesfatin-1: A Biomarker and Potential Therapeutic Target in Neurological Disorders.

Nesfatin-1 is a novel adipocytokine consisting of 82 amino acids with anorexic and anti-hyperglycemic properties. Further studies of nesfatin-1 have shown it to be closely associated with neurological disorders. Changes in nesfatin-1 levels are closely linked to the onset, progression and severity of neurological disorders. Nesfatin-1 may affect the development of neurological disorders and can indicate disease evolution and prognosis, thus informing the choice of treatment options. In addition, regulation of the expression or level of nesfatin-1 can improve the level of neuroinflammation, apoptosis, oxidative damage and other indicators. It is demonstrated that nesfatin-1 is involved in neuroprotection and may be a therapeutic target for neurological disorders. In this paper, we will also discuss the role of nesfatin-1 as a biomarker in neurological diseases and its potential mechanism of action in neurological diseases, providing new ideas for the diagnosis and treatment of neurological diseases.