Protein Carbonyl Levels Research Articles

Green tea beverage protects against thiabendazole-induced kidney and liver injury through antioxidant actions in rats in vivo

ABSTRACT Thiabendazole (TBZ) is an important molecule used in several different areas. Two percent of green tea leaf extracts (GTE) obtained by maceration were tested against TBZ-induced liver and kidney toxicity, by using four groups of male Wistar rats controls, control-tea (2%), TBZ-treated, and TBZ+GTE. The results revealed, after 4 weeks of treatment, an increase in nitric oxide (NO), advanced oxidation protein products (AOPP) and protein carbonyl (PC) levels and a decrease in catalase activity in the tissues homogenates on TBZ-treated rats. The administration of GTE to TBZ-treated rats attenuated the increase in NO, AOPP and PC levels and improved activities of catalase and markers. Histological examination demonstrated marked tissue damage in the liver and kidney of TBZ-treated animals. Co-administration of TBZ and green tea reduced tissue damage. Acute exposure to TBZ leads to acute inflammation through oxidant – antioxidant imbalance. GTE could therefore be a useful therapeutic option for reversing TBZ-induced oxidative stress.

Storage causes protein oxidation of soybean meal and affects antioxidant status, digestive performance and meat quality of broilers.

This study investigated the protein oxidation of soybean meal (SBM) stored in a warehouse and the effects of SBM on growth performance, antioxidant status, digestive performance, intestinal morphology, and breast muscle quality of broilers. In total, 160 one-day-old Arbor Acres Plus broilers (half male and half female) were randomly divided into two groups with ten replicates of eight birds each: The control group was served with a basal diet including SBM stored at -20 °C (FSBM), and the experimental group was served with a basal diet including SBM stored in a warehouse at room temperature for 45 days (RSBM). Compared with FSBM, the protein carbonyl level in RSBM was increased, the free and total thiol levels and in vitro digestibility of protein were decreased. The RSBM decreased the serum glutathione (GSH) level and the hepatic total superoxide dismutase (T-SOD) activity at days 21 and 42 when compared with FSBM. Further, RSBM reduced the duodenal T-SOD activity, jejunal catalase (CAT), and T-SOD activities at day 21, and decreased the duodenal CAT and T-SOD activities, jejunal T-SOD activity, and ileal GSH level and T-SOD activity at days 21 and 42 when compared with FSBM. Besides, the trypsin activity and the ratio of villus height (VH) to crypt depth (CD) in small intestines of broilers at days 21 and 42 were reduced when fed with a RSBM-contained diet. Compared with FSBM, the 24-h drip loss, shear force, and 24- and 48-h cooking loss of breast muscle were increased of RSBM group, the opposite result was observed for muscle lightness at 48 h. Room temperature storage for 45 days led a protein oxidation and decreased in vitro digestibility in SBM, and fed RSBM impaired growth performance, antioxidant status, and meat quality, reduced trypsin activity, and affected the small intestine morphologyin broilers.

Curcumin Attenuates Doxorubicin-Induced Cardiac Oxidative Stress and Increases Survival in Mice.

Doxorubicin (DOX) is a potent chemotherapeutic agent used to treat multiple types of cancer, but its clinical application is limited by cardiotoxicity, mainly due to oxidative stress. Curcumin (CUR) is a natural polyphenolic compound with strong antioxidant properties, but its potential protective effects against DOX-induced cardiotoxicity need further investigation. This study aimed to evaluate CUR's efficacy in mitigating DOX-induced oxidative stress in the hearts of BALB/c mice. Mice received a DOX dose of 9 mg/kg or 16 mg/kg; half of the mice received daily doses of 100 mg/kg CUR for 15 days. Survival analysis, histopathological examination, and oxidative stress markers were assessed to determine the cardioprotective effects of CUR. Results showed that CUR significantly reduced oxidative damage and improved survival rates, particularly at the lower DOX dose (9 mg/kg). Mice treated with DOX-9 mg/kg plus CUR showed improved health conditions and reduced levels of reactive oxygen species (ROS), lipid peroxidation, sulfhydryl production, and protein carbonylation. Histopathological analysis confirmed reduced cardiac tissue damage. In conclusion, CUR combined with a lower dose of DOX effectively reduces oxidative stress and cardiac injury, enhancing survival in BALB/c mice. These findings suggest that CUR is a promising adjunct therapy to mitigate DOX-induced cardiotoxicity, potentially improving the DOX therapeutic index in cancer treatment.

Effects of sulfamethazine and tetracycline at molecular, cellular and tissue levels in Eisenia fetida earthworms

Soil contamination by antibiotics is a global issue of great concern that contributes to the rise of bacterial antibiotic resistance and can have toxic effects on non-target organisms. This study evaluated the variations of molecular, cellular, and histological parameters in Eisenia fetida earthworms exposed to sulfamethazine (SMZ) and tetracycline (TC), two antibiotics commonly found in agricultural soils. The earthworms were exposed for 14 days to a series of concentrations (0, 10, 100, and 1000 mg/kg) of both antibiotics. SMZ and TC did not affect the survival of E. fetida, however, other effects at different levels of biological complexity were detected. The two highest concentrations of SMZ reduced the viability of coelomocytes. At the highest TC concentration, there was a noticeable decline in cell viability, acetylcholinesterase activity (neurotoxicity), and the relative presence of mucopolysaccharides in the epidermis (mucous production). Glutathione S-transferase activity decreased in all TC treatments and at the highest SMZ concentration. However, levels of malondialdehyde and protein carbonyls did not change, suggesting an absence of oxidative stress. Tetracycline was neurotoxic to E. fetida and changed the integrity of the epidermis. Both antibiotics altered the intestinal microbiota of E. fetida, leading to a reduction in the relative abundance of bacteria from the phyla Proteobacteria and Bacteroidetes, while causing an increase in the phylum Actinobacteroidota. All observed changes indicate that both SMZ and TC can disrupt the earthworms' immune system and gut microbiome, while fostering the growth of bacteria that harbour antibiotic resistance genes. Finally, both antibiotics exerted additional metabolic and physiological effects that increased the vulnerability of E. fetida to pathogens.

Exploring oxysterols and protein carbonylation in cervicovaginal secretions as biomarkers for cervical cancer development

Cervical cancer, a major global health issue and the fourth most common cancer among women, is strongly linked to Human Papillomavirus (HPV) infection. Emerging evidence indicates that oxidative stress plays a critical role in the carcinogenesis of cervical tissue. This study investigates the relationship between oxidative stress markers—specifically oxysterols, lipid oxidation, and protein carbonylation—and the progression of cervical neoplasia.Oxysterols, which are elevated in various inflammatory diseases and cancers, were measured in cervicovaginal fluid samples using LC-MS/MS. The targeted oxysterols included 27-hydroxycholesterol (27-OHC), 7β-hydroxycholesterol (7β-OHC), 7-ketocholesterol (7-KC), and 7α,27-dihydroxycholesterol (7α,27-diOHC). Among these, 7α,27-dihydroxycholesterol was significantly increased in correlation with the severity of neoplastic stages. In parallel, protein carbonylation, an indicator of cellular oxidative stress, was assessed. Results revealed higher levels of protein carbonylation in neoplastic samples compared to non-neoplastic controls. These modifications were further analysed through redox proteomics to identify the specific proteins affected.The study demonstrates that elevated lipid oxidation and protein carbonylation in cervicovaginal secretions are linked to the development and progression of cervical cancer. Identifying these biomarkers may improve screening strategies, enabling the identification of individuals at increased risk for cervical neoplasia and guiding timely interventions.

Exposure to different cobalt chloride levels produces oxidative stress and lipidomic changes and affects the liver structure of Cyprinus carpio juveniles.

The present investigation was undertaken to evaluate the toxic effects of CoCl2-induced hepatotoxicity and fatty acid changes in juvenile Cyprinus carpio. Fish were divided into six experimental groups in duplicate. The first group served as controls. The second group received the lowest exposure dose at 2.5µg/L. In the third group, fish were exposed to 25µg/L of CoCl2. The fourth group was exposed to 50µg/L of CoCl2. The last two groups were exposed to the highest doses, 100 and 500µg/L of CoCl2. Total antioxidant activities were estimated using a colorimetric method. Liver fatty acid compositions were analyzed by high-performance gas chromatography (GC). Hepatopathy was identified through microscopic analysis. Exposure of C. carpio to CoCl2 resulted in hepatotoxicity, indicated by increased levels of malondialdehyde (MDA), hydrogen peroxide (H2O2), protein carbonyls (PCO), and alterations in the ferric reducing antioxidant power system (FRAP). Superoxide dismutase (SOD), glutathione-S-transferase (GST), glutathione peroxidase (GPx), reduced glutathione (GSH), metallothioneins (MTs), and low thiol levels (L-SH) significantly increased, particularly under exposure to the highest CoCl2 doses (100 and 500µg/L). Acetylcholinesterase activity decreased significantly in C. carpio exposed to graded CoCl2 doses. Additionally, there was a decrease in polyunsaturated fatty acids (PUFA), primarily n-3 PUFA, docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), while an increase in monounsaturated (MUFA) and saturated fatty acids (SFA), including palmitic (C16:0), stearic (C18:0), palmitoleic (C16:1), and oleic (C18:1) acids, was observed. Histopathological examination of the liver confirmed hepatopathy revealing characteristic tissue changes such as leucocyte infiltration, hepatic cell membrane degradation, vacuolization, and lipid inclusions. The study provided ethnophysiology insights into the responses of C. carpio to CoCl2-induced oxidative stress and lipidomic alteration, underscoring its potential as a bioindicator for assessing environmental impacts and metal contamination.

The effect of Polygonum hyrcanicum Rech. f. hydroalcoholic extract on oxidative stress and nephropathy in alloxan-induced diabetic mice

Diabetic nephropathy, characterized by inflammation and oxidative stress, poses a management challenge. This study investigates the effect of Polygonum hyrcanicum extract on diabetic nephropathy in alloxan-induced diabetic mice. In this experimental animal study, the P. hyrcanicum extract was prepared using continuous macerations. Thirty male Albino mice, divided into five groups, were induced with alloxan-induced diabetes. They received intraperitoneal injections of the plant extract (100 and 200 mg/kg) and metformin (300 mg/kg) for four weeks. Kidney and blood samples were collected to assess protein carbonyl, glutathione, lipid peroxidation, TNF-α and IL-6 levels. The amount of total flavonoid and phenolic content in the hydroalcoholic extract of P. hyrcanicum were 7.5 ± 0.3 mg of quercetin and 88.2 ± 1.3 mg gallic acid per gram of extract respectively. The antioxidant activity level of the hydroalcoholic extract was determined to be 1.78 ± 0.51 mM equivalent per gram of extract. Alloxan administration resulted in a significant reduction in glutathione levels and a significant increase in protein carbonyl, lipid peroxidation, TNF-α, and IL-6 levels. Hydroalcoholic extract of P. hyrcanicum effectively reduced oxidative stress markers and inflammatory cytokines (TNF-α, IL-6), indicating its potential in mitigating diabetic nephropathy. However, no significant difference in efficacy was observed between the 100 mg/kg and 200 mg/kg doses in terms of reducing these toxicities.

Combining In Vitro, In Vivo, and Network Pharmacology Assays to Identify Targets and Molecular Mechanisms of Spirulina-Derived Biomolecules against Breast Cancer.

The current research employed an animal model of 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary gland carcinogenesis. The estrogen receptor-positive human breast adenocarcinoma cell line (MCF-7) was used for in vitro analysis. This was combined with a network pharmacology-based approach to assess the anticancer properties of Spirulina (SP) extract and understand its molecular mechanisms. The results showed that the administration of 1 g/kg of SP increased the antioxidant activity by raising levels of catalase (CAT) and superoxide dismutase (SOD), while decreasing the levels of malonaldehyde (MDA) and protein carbonyl. A histological examination revealed reduced tumor occurrence, decreased estrogen receptor expression, suppressed cell proliferation, and promoted apoptosis in SP protected animals. In addition, SP disrupted the G2/M phase of the MCF-7 cell cycle, inducing apoptosis and reactive oxygen species (ROS) accumulation. It also enhanced intrinsic apoptosis in MCF-7 cells by upregulating cytochrome c, Bax, caspase-8, caspase-9, and caspase-7 proteins, while downregulating Bcl-2 production. The main compounds identified in the LC-MS/MS study of SP were 7-hydroxycoumarin derivatives of cinnamic acid, hinokinin, valeric acid, and α-linolenic acid. These substances specifically targeted three important proteins: ERK1/2 MAPK, PI3K-protein kinase B (AKT), and the epidermal growth factor receptor (EGFR). Network analysis and molecular docking indicated a significant binding affinity between SP and these proteins. This was verified by Western blot analysis that revealed decreased protein levels of p-EGFR, p-ERK1/2, and p-AKT following SP administration. SP was finally reported to suppress MCF-7 cell growth and induce apoptosis by modulating the PI3K/AKT/EGFR and MAPK signaling pathways suggesting EGFR as a potential target of SP in breast cancer (BC) treatment.

Extracellular Vesicles from hiPSC-derived NSCs Protect Human Neurons against Aβ-42 Oligomers Induced Neurodegeneration, Mitochondrial Dysfunction and Tau Phosphorylation.

One of the hallmarks of Alzheimer's disease (AD) is the buildup of amyloid beta-42 (Aβ-42) in the brain, which leads to various adverse effects. Therefore, therapeutic interventions proficient in reducing Aβ-42-induced toxicity in AD are of great interest. One promising approach is to use extracellular vesicles from human induced pluripotent stem cell-derived neural stem cells (hiPSC-NSC-EVs) because they carry multiple therapeutic miRNAs and proteins capable of protecting neurons against Aβ-42-induced pathological changes. Therefore, this in vitro study investigated the proficiency of hiPSC-NSC-EVs to protect human neurons derived from two distinct hiPSC lines from Aβ-42o-induced neurodegeneration. We isolated hiPSC-NSC-EVs using chromatographic methods and characterized their size, ultrastructure, expression of EV-specific markers and proficiency in getting incorporated into mature human neurons. Next, mature human neurons differentiated from two different hiPSC lines were exposed to 1 µM Aβ-42 oligomers (Aβ-42o) alone or with varying concentrations of hiPSC-NSC-EVs. The protective effects of hiPSC-NSC-EVs against Aβ-42o-induced neurodegeneration, increased oxidative stress, mitochondrial dysfunction, impaired autophagy, and tau phosphorylation were ascertained using multiple measures and one-way ANOVA with Newman-Keuls multiple comparisons post hoc tests. Significant neurodegeneration was observed when human neurons were exposed to Aβ-42o alone. Notably, neurodegeneration was associated with elevated levels of oxidative stress markers malondialdehyde (MDA) and protein carbonyls (PCs), increased expression of proapoptotic Bax and Bad genes and proteins, reduced expression of the antiapoptotic gene and protein Bcl-2, increased expression of genes encoding mitochondrial complex proteins, decreased expression of autophagy-related proteins Beclin-1 and microtubule-associated protein 1 light chain 3B, and increased phosphorylation of tau. However, the addition of an optimal dose of hiPSC-NSC-EVs (6 x 10 9 EVs) to human neuronal cultures exposed to Aβ-42o significantly reduced the extent of neurodegeneration, along with diminished levels of MDA and PCs, normalized expressions of Bax, Bad, and Bcl-2, and genes linked to mitochondrial complex proteins, and reduced tau phosphorylation. The findings demonstrate that an optimal dose of hiPSC-NSC-EVs could significantly decrease the degeneration of human neurons induced by Aβ-42o. The results also support further research into the effectiveness of hiPSC-NSC-EVs in AD, particularly their proficiency in preserving neurons and slowing disease progression.

Circadian rhythms of antioxidant enzymes activity, clock, and inflammation factors are disrupted in the prefrontal cortex of aged rats. Potential targets for therapeutic strategies for a healthy aging.

Age impairs cognitive functions and antioxidant defenses, for example, by increasing oxidative stress and inflammation in the brain. However, so far, there is no report on the consequences of aging on temporal patterns of proteins and lipids oxidation, antioxidant enzymes activity, endogenous clock and proinflammatory cytokine, in the prefrontal cortex (PFC). Therefore, our objectives here were: 1) to investigate the endogenous nature of 24h-rhythms of lipoperoxidation, protein carbonyls levels, CAT and GPx activity, RORa, and TNFα, in the rat PFC, and 2) to study the consequences of aging on the circadian organization of those factors in the same brain area. To do that, 3- and 22-mo-old male Holtzman rats were maintained under constant darkness conditions during 15 days before reaching the corresponding age. PFC samples were isolated every 4 h, under dim-red light, during a 24h period. Our results revealed circadian patterns of antioxidant enzymes activity, oxidative stress, RORa and TNFα proteins levels, in the PFC of young rats. The circadian distribution of the rhythms’ phases suggests the existence of a reciprocal communication among the antioxidant defenses, the endogenous clock, and the inflammation, in the PFC. Noteworthy, such circadian organization disappears in the PFC of aged rats. An increased oxidative stress would make the redox environment to change into an oxidative status, which alters the endogenous clock activity and disrupts the circadian organization of, at least part, of the antioxidant defenses and the TNFα, in the PFC. These results might highlight novel chronobiological targets for the design of therapeutic strategies addressed to a healthy aging.

Elevated plasma protein carbonylation increases the risk of ischemic cerebrovascular events in patients with atrial fibrillation: association with a prothrombotic state.

Plasma protein carbonylation that reflects oxidative stress has been demonstrated to be associated with the prothrombotic fibrin clot phenotype. However, the role of protein carbonyls (PC) in predicting ischemic stroke in atrial fibrillation (AF) is largely unknown. This study aimed to investigate whether PC increase the risk of stroke in anticoagulated AF patients during follow-up. In 243 AF patients on anticoagulation (median age 69years; median CHA2DS2-VASc of 4), we measured plasma PC using the assay by Becatti, along with plasma clot permeability (Ks), clot lysis time (CLT), thrombin generation, and fibrinolytic proteins, including plasminogen activator inhibitor type 1 (PAI-1) and thrombin activatable fibrinolysis inhibitor (TAFI). Ischemic stroke, major bleeding, and mortality were recorded during a median follow-up of 53months. Plasma PC levels (median, 3.16 [2.54-3.99] nM/mg protein) at baseline showed positive associations with age (P < 0.001), CHA2DS2-VASc (P = 0.003), and N-terminal B-type natriuretic peptide (P = 0.001), but not with type of AF or comorbidities except for heart failure (P = 0.007). PC levels were correlated with CLT (r = 0.342, P < 0.001), endogenous thrombin potential (r = 0.217, P = 0.001) and weakly with Ks (r = -0.145, P = 0.024), but not with fibrinogen, PAI-1, or TAFI levels. Stroke was recorded in 20 patients (1.9%/year), who had at baseline 36% higher PC levels (P < 0.001). Elevated PC (P = 0.003) at baseline were independently associated with stroke risk. Our findings suggest that in patients with AF enhanced protein carbonylation is associated with increased "residual" risk of stroke despite anticoagulation, which is at least in part due to unfavorably altered fibrin clot phenotype.

Indole-3-carbinol loaded-nanocapsules modulated inflammatory and oxidative damages and increase skin wound healing in rats

This study evaluated the effects of topically applied hydrogels (HG) containing nanoencapsulated indol-3-carbinol (I3C) and its free form in a rat model of skin wounds. Formulations were topically applied twice a day for five days to the wounds. On days 1, 3, and 6, the wound area was measured to verify the % of regression. On the sixth day, the animals were euthanized for the analysis of the inflammatory and oxidative profile in wounds. The nanocapsules (NC) exhibited physicochemical characteristics compatible with this kind of suspension. After five hours of exposure to ultraviolet C, more than 78% of I3C content in the suspensions was still observed. The NC-I3C did not modify the physicochemical characteristics of HG when compared to the HG base. In the in vivo study, an increase in the size of the wound was observed on the 3rd experimental day, which was lower in the treated groups (mainly in HG-NC-I3C) compared to the control. On the 6th day, HG-I3C, HG-NC-B, and HG-NC-I3C showed lower regression of the wound compared to the control. Additionally, HG-NC-I3C exhibited an anti-inflammatory effect (as observed by decreased levels of interleukin-1B and myeloperoxidase), reduced oxidative damage (by decreased reactive species, lipid peroxidation, and protein carbonylation levels), and increased antioxidant defense (by improved catalase activity and vitamin C levels) compared to the control. The current study showed more satisfactory results in the HG-NC-I3C group than in the free form of I3C in decreasing acute inflammation and oxidative damage in wounds.

Anti-inflammatory and anti-angiogenic effects of Withania somnifera extract on liver toxicity induced by silver nanoparticles in vivo.

The liver is a critical organ in the human body and is frequently exposed to numerous exogenous toxic substances, including silver nanoparticles (AgNPs). This study aimed to examine the anti-inflammatory, anti-angiogenic, and hepatoprotective effects of Withania somnifera (W. somnifera) extract on AgNP-induced liver toxicity in Swiss mice. Fifty mice were divided into five groups. Group I (negative control) consisted of ten mice. Group II received oral W. somnifera extracts (80 mg/kg/bw) for 14 days. Group III was injected intraperitoneally (i.p.) with AgNPs at a daily dose of 35 mg/kg/bw for 3 days. Group IV received i.p. AgNPs for 3 days, followed by saline for 14 days. Group V received i.p. AgNPs for 3 days, followed by oral W. somnifera (80 mg/kg/bw) for 14 days. Liver function tests, pro and anti-inflammatory cytokines, antioxidant activities, protein carbonyl (PC) levels, liver histopathological analysis, immunohistochemical expressions of transcription factor (NF-κB), and vascular endothelial growth factor (VEGF) were examined. Group III had elevated levels of liver function, a significant increase of pro and anti-inflammatory cytokines, antioxidant activity, and PC levels. Histological observations revealed congested sinusoids filled with red blood cells (RBCs) and hepatocyte necrosis. Also, positive expressions of NF-κB and VEGF were detected compared with Group I. However, the administration of W. somnifera to Group V revealed significant changes with evident improvements in liver function biomarkers, pro and anti-inflammatory cytokines, antioxidant activities, oxidative stress markers (PC), and histopathological and immunohistochemical parameters compared to Group III. The results revealed that W. somnifera has promising and potential hepatoprotective, anti-inflammatory, and anti-angiogenic effects against liver toxicity. Further detailed studies are recommended to explore the potential of W. somnifera as a treatment for human liver ailments.

Impact of Gliclazide Modified Release or Glimepiride as Add-on Therapy to Metformin on Glycemic and Oxidative Stress Parameters in Type 2 Diabetic Patients

Background: Type 2 diabetes mellitus is a condition characterized by an elevation of oxidative stress, which has been implicated in diabetic progression and its vascular complications. Aim: Assessing the impact of gliclazide modified release (MR) versus glimepiride on oxidative stress markers, glycemic indices, lipid profile, and estimated glomerular filtration rate in uncontrolled type 2 diabetic patients on metformin monotherapy. Methods: This was an observational comparative study conducted in Thi-Qar specialized diabetic, endocrine, and metabolism center. Sixty-six patients were randomized into two groups based on the addition of the sulfonylureas (SUs). Group 1 (33 patients) was on gliclazide MR, whereas Group 2 (33 patients) was on glimepiride. The measured oxidative stress markers were reduced glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), and protein carbonyl (PC) evaluated before and after 16 weeks of SUs addition. Results: There were significant drops in SOD (P &lt; 0.001), MDA (P &lt; 0.001), and PC (P = 0.001) and a significant increase in GSH (p = 0.029) levels after gliclazide MR add-on therapy. There were significant drops in SOD (P = 0.026) and MDA (P &lt; 0.001) levels with non-significant changes in both GSH (P = 0.214) and PC (P = 0.538) after glimepiride add-on therapy. There was a significant difference in improvement of PC level (P = 0.048) in the gliclazide group compared to the glimepiride group, with a non-significant numerically higher improvement of GSH, SOD, and MDA in gliclazide MR than glimepiride. At the end of the study, there were no significant differences in glycemic control, lipid profile, or eGFR improvement between the two groups. Conclusion: Glycemic control plays a pivotal role in decreasing oxidative stress. The control of diabetes with the gliclazide-MR-metformin combination reduced oxidative stress more than the glimepiride-metformin combination, indicating its antioxidant property. Keywords: Oxidative Stress, T2DM, Gliclazide MR, Glimepiride, Metformin.

The combined effect of morin and hesperidin on memory ability and oxidative/nitrosative stress in a streptozotocin-induced rat model of Alzheimer’s disease

Alzheimer's disease (AD), the most frequent neurodegenerative disease within dementias, affects the CNS, leading to gradual memory issues and cognitive dysfunction. Oxidative stress in AD contributes to ongoing neuronal loss and hastens disease progression. Notably, the potent antioxidant compounds morin and hesperidin have demonstrated significant effectiveness in addressing oxidative stress. This study explores the impact of morin and hesperidin on behavior and oxidative stress in the streptozotocin (STZ)-induced AD rat model. The experiment involved five groups: control, STZ, STZ+morin, STZ+hesperidin, and STZ+morin+hesperidin. The rat model of AD was created by injecting STZ with the stereotaxic surgery. Morin and hesperidin were applied to the groups for 7-days. After the applications, the Morris water maze (MWM) and novel object recognition (NOR) tests were used and the rats were sacrificed. Malondialdehyde (MDA), glutathione (GSH), nitric oxide (NOx), and protein carbonyl (PC) levels were measured. In the STZ group, the levels of NOx and PC exhibited a noteworthy increase compared to the control. Conversely, the application of morin and/or hesperidin treatments reduced NOx and PC levels compared to the STZ group. The co-administration of morin and hesperidin improved the antioxidant status and decreased lipid peroxidation in STZ-induced rats. In the STZ group, serum advanced oxidation protein products (AOPP) levels were statistically elevated compared to the control. However, in the treatment groups, morin and/or hesperidin successfully decreased AOPP levels to those observed in the control. The combined use of these flavonoids may have a neuroprotective effect regarding memory problems and decreasing oxidative/nitrosative stress.

Effects of chronic intermittent cold stress on anxiety-depression-like behaviors in adolescent rats

Stress, which triggers numerous physiological and behavioral responses in the organism, is a significant risk factor that contributes to the development of psychiatric disorders such as depression and anxiety. This study aimed to investigate the inflammation, oxidative stress status, anxiety, and depression-like behaviors of adolescent rodents exposed to chronic intermittent cold stress. Adolescent male rats were subjected to a modified chronic intermittent cold stress model (21 days, 1 hour/day, 4 °C). Depression-like behaviors were evaluated using the sucrose preference and forced swimming tests, while anxiety-like behaviors were assessed using the open field, elevated plus maze, and light-dark box tests. We measured levels of cortisol, tumor necrosis factor-α, interleukin-1β, brain-derived natriuretic factor, reactive oxygen species, malondialdehyde, total oxidants and antioxidants, and other chemicals in the prefrontal cortex, thalamus, striatum, and hippocampus brain regions of rats using ELISA and colorimetric methods. Data were analyzed using Student’s t-test and Pearson correlation analysis. After the cold stress treatment, both anxiety and depression-like behaviors increased remarkably in the subjects. Our study revealed significant changes in various brain regions among the stress-exposed subjects. Cold stress resulted in decreased BDNF levels in the prefrontal cortex and striatum (p < 0.05), increased cortisol levels in the prefrontal cortex (p < 0.05), increased IL-1β levels in the hippocampus and thalamus (p < 0.05), increased protein carbonyl levels in the striatum (p < 0.05), and decreased TAS in the prefrontal cortex and thalamus (p < 0.05). Adolescent rats exposed to cold exhibit both anxiety- and depression-like behaviors. This study observed an increase in inflammation in various brain regions, yet the responses to stress varied. Our findings suggest that adolescence is a period of heightened sensitivity to stress, which can lead to dramatic consequences.

Sex-Related Differences in Oxidant and Antioxidant Profiles of Murine Kidney and Brain: A Focus on Sirt3-Mediated Regulation

Background: Sirt3 is a mitochondrial deacetylase with an important role in maintainance of cellular redox and metabolic homeostasis and mitochondrial function. As growing evidence support the existence of sex-specific responses to metabolic and oxidative stress, we aimed to investigate sex- and organ-specific effects of Sirt3 loss. Materials and methods: Expression of Sirt3, PGC-1a, CuZnSOD, MnSOD and Cat proteins in kidneys and brains of Sirt3-wild type (Sirt3 WT) and Sirt3-knockout (Sirt3 KO) mice was assessed by Western blotting. Protein carbonylation and lipid peroxidation levels were measured using ELISA and fluorometric assays, respectively. SOD and Cat activities were determined using standard enzymatic assays. Results: Significant sex- and organ- specific differences in response to Sirt3 loss were detected. Sirt3 knockout affected kidneys more than brain tissue, with females showing lower levels PC and LPO. In kidneys, female KO showed higher MnSOD, but lower CuZnSOD and Cat activity compared to males. In brains, WT females show higher activities of these enzymes than males, suggesting a sex-specific protection mechanism, but female KO brains show a larger decrease in these parameters. Conclusion: Our study provides comprehensive insights into the complex interplay of Sirt3, oxidative stress, and antioxidant defenses in murine kidney and brain. The observed differences between the two organs and the impact of sex highlight the need for studying Sirt3 function in diverse physiological contexts. The tissue-specific responses and sex-related variations underscore the importance of considering these factors in the development of therapeutic strategies targeting mitochondrial function and redox homeostasis.

The Interactive Effects of the Anti-Sea Lice Pesticide Azamethiphos and Temperature on Oxidative Damage and Antioxidant Responses in the Oyster Ostrea chilensis.

Azamethiphos is used in the salmon industry to treat sea lice and is subsequently discharged into the sea, which may affect non-target species (NTS). A rise in seawater temperature could enhance the sensitivity of NTS. Thus, in the present investigation, the combined effects of azamethiphos (0 µg L-1, 15 µg L-1 and 100 µg L-1) and temperature (12 °C and 15 °C) was assessed over time (7 days) in the gonads and gills of the oyster Ostrea chilensis, assessing its oxidative damage (lipid peroxidation and protein carbonyls) and total antioxidant capacity. Our results indicated that in gonads and gills, lipid peroxidation levels increased over time during exposure to both pesticide concentrations. Protein carbonyl levels in gills increased significantly in all experimental treatments; however, in gonads, only pesticide concentration and exposure time effected a significant increase in protein damage. In both, gill and gonad temperature did not influence oxidative damage levels. Total antioxidant capacity in gonads was influenced only by temperature treatment, whereas in the gills, neither temperature nor azamethiphos concentration influenced defensive responses. In conclusion, our results indicated the time of pesticide exposure (both concentrations) had a greater influence than temperature on the cellular damage in this oyster.

Exposure to pesticides used in rice farming (bentazone, chlorantraniliprole and tebuconazole) affects biochemical biomarkers and hepatic histopathological parameters of hammertoad tadpoles (Boana faber)

Pesticides used in rice cultivation can cause negative health effects to non-target organisms representative of natural biodiversity. In this context, the present study aimed to investigate the occurrence of pesticides in surface waters from a river that flows in the middle of a rice farming-dominated area. We were also interested in evaluate biochemical and histological effects caused by exposure (16 d) to the lower and higher concentrations of the main found herbicide (bentazone, BTZ), insecticide (chlorantraniliprole, CTP) and fungicide (tebuconazole, TBZ), isolated or mixed, in Boana faber tadpoles. No significant differences were observed in the development of the animals. Tadpoles exposed to the herbicide BTZ showed higher hepatic levels of malondialdehyde (MDA). In animals exposed to CTP, MDA levels were lower than controls. Animals exposed to the fungicide TBZ showed higher hepatic activity of glutathione S-transferase and carboxylesterase (CbE), as well as higher levels of carbonyl proteins and MDA. Animals exposed to Mix showed higher activity in CbE and glucose-6-phosphate dehydrogenase activity in the liver, as well as higher levels of MDA. In the brain and muscle of tadpoles exposed to Mix, acetylcholinesterase activity was higher. Histological changes were also observed in pesticide-exposed animals, such as increased occurrence of melanomacrophages, inflammatory infiltrates and congestion. Our data evidences the contamination of natural aquatic environments by rice pesticides, and the adverse effects of main ones in B. faber tadpoles, which suggests the contribution of pesticides derived from rice cultivation to the degradation of local biodiversity health.

Assessing the multi-dimensional impact of lead-induced toxicity on collembola found in maize fields: From oxidative stress to genetic disruptions

The prolonged exposure of agricultural soils to heavy metals from wastewater, particularly in areas near industrial facilities, poses a significant threat to the well-being of living organisms. The World Health Organization (WHO) has established standard permissible limits for heavy metals in agricultural soils to mitigate potential health hazards. Nevertheless, some agricultural fields continue to be irrigated with wastewater containing industrial effluents. This study aimed to assess the concentration of lead in soil samples collected from agricultural fields near industrial areas. Subsequently, we determined the lethal concentration (LC50) of lead (Pb) and other heavy metals for two Collembola species, namely Folsomia candida, a standard organism for soil ecotoxicity tests, and comparing it with Proisotoma minuta. The research further examined the toxic effects of lead exposure on these two species, revealing depletion in the energy reservoirs and alterations in the tissue histology of both organisms. The study revealed that lead can induce genotoxic damage as it evidently has moderate binding affinity with the ct-DNA and hence can cause DNA fragmentation and the formation of micronuclei. Elevated lipid peroxidation (LPO) levels and protein carbonylation levels were observed, alongside a reduction in antioxidant enzymes (CAT, SOD & GPx). These findings suggest that lead disrupts the balance between oxidants and the antioxidant enzyme system, impairing defense mechanisms and consequential derogatory damage within microarthropods. The investigation elucidates a complex network of various signaling pathways compromised as a result of lead toxicity. Hence, it presents a novel perspective that underscores the pressing necessity for implementing an integrated risk assessment framework at the investigated site.