Decrease In Antioxidant Capacity Research Articles

Local Application of Tanshinone IIA protects mesenchymal stem cells from apoptosis and promotes fracture healing in ovariectomized mice

BackgroundElderly patients suffering from osteoporotic fractures are more susceptible to delayed union or nonunion, and their bodies then are in a state of low-grade chronic inflammation with decreased antioxidant capacity. Tanshinone IIA is widely used in treating cardiovascular and cerebrovascular diseases in China and has anti-inflammatory and antioxidant effects. We aimed to observe the antioxidant effects of Tanshinone IIA on mesenchymal stem cells (MSCs), which play important roles in bone repair, and the effects of local application of Tanshinone IIA using an injectable biodegradable hydrogel on osteoporotic fracture healing.MethodsMSCs were pretreated with or without different concentrations of Tanshinone IIA followed by H2O2 treatment. Ovariectomized (OVX) C57BL/6 mice received a mid-shaft transverse osteotomy fracture on the left tibia, and Tanshinone IIA was applied to the fracture site using an injectable hydrogel.ResultsTanshinone IIA pretreatment promoted the expression of nuclear factor erythroid 2-related factor 2 and antioxidant enzymes, and inhibited H2O2-induced reactive oxygen species accumulation in MSCs. Furthermore, Tanshinone IIA reversed H2O2-induced apoptosis and decrease in osteogenic differentiation in MSCs. After 4 weeks of treatment with Tanshinone IIA in OVX mice, the bone mineral density of the callus was significantly increased and the biomechanical properties of the healed tibias were improved. Cell apoptosis was decreased and Nrf2 expression was increased in the early stage of callus formation.ConclusionsTaken together, these results indicate that Tanshinone IIA can activate antioxidant enzymes to protect MSCs from H2O2-induced cell apoptosis and osteogenic differentiation inhibition. Local application of Tanshinone IIA accelerates fracture healing in ovariectomized mice.

Decreased antioxidant capacity in children with diabetic ketoacidosis

Objective. To analyze the levels of antioxidant enzyme superoxide dismutase (SOD) and glutathione peroxidase (GP) against the background of diabetic ketoacidosis (DKA) in type 1 diabetes mellitus (DM) children and adolescents. Materials and methods. The study involved examination of 74 children: 50 DKA children (study group) and 24 relatively healthy children (control group). The study group children were divided into two subgroups: subgroup 1 included children with DKA against the background of type 1 DM onset (n=27), subgroup 2 consisted of children with DKA against the background of chronic type 1 DM (n=23). SOD and GP concentrations in blood plasma were determined in all children by enzyme immunoassay. The reliability between the data was estimated using the Mann-Whitney test, Kruskal-Wallis test and Spearman coefficient. Results. A significant decrease in SOD and GP in children with DKA was revealed as follows: 13130 [13005–18255] Pg/ml and 50.085 [42.02–70.325] Ng/ml, compared to controls: 16415 [13370–19935] Pg/ml and 84.695 [52.49–144.5] Ng/ml, respectively. Minimal SOD and GP were noted in patients with DKA at the background of chronic type 1 DM, compared to DM onset children. The study indicates a reliable correlation between age, duration of the disease, number of DKA in the history and low values of SOD and GP. Conclusion. Decreased antioxidant capacity was found in children with DKA in type 1 DM. SOD and GP can be considered in pediatric practice as markers of oxidative stress in DKA. In addition, an early detection of SOD and GP contributes to the efficient therapy of DKA in children and adolescents.

Gestational Long Term High-Altitude Hypoxia and Metabolomic Reprogramming in Uterine Arteries of Adult Sheep

Long term hypoxic stress during pregnancy causes a reduction in uterine blood flow, compromising oxygen and nutrient delivery to the fetus. There are multiple epigenetic factors involved in the structural and functional impairments that underlie the impairments in uterine arterial function. Evidence indicates that oxidative stress plays an important role to the decrements in blood flow following high altitude pregnancy. The purpose of the current study was to test the hypothesis that changes in oxylipin and endocannabinoid signaling are important to the increases in oxidative stress along with changes in glucose and fat metabolism. To further understand the mechanisms associated with disruption of uterine artery blood flow due to high altitude pregnancy, we examined a high altitude pregnant sheep model. Pregnant and non-pregnant sheep were housed either at low (700m) or high altitude (3801 meters) for 110+ days of pregnancy. Uterine arteries were excised from pregnant and non-pregnant sheep and targeted as well as untargeted metabolomic analyses were performed to test the hypothesis that hypoxia increases oxidative stress and reduces oxidative metabolism. Enrichment analysis of the metabolites show that hypoxia impacted several key biochemical pathways. At high altitude there were decreases in Alpha Linolenic Acid and Linoleic Acid Metabolism along with reductions in Pyruvate Metabolism and antioxidants. Further to this, there was an increase in the metabolism of Arachidonic Acid, Glycerolipids, and Methionine, which are linked to inflammation, cell signaling, and cell growth. Fully understanding how increased oxidative stress and inflammatory pathways along with decreased antioxidant capacity and changes in cellular metabolism is tied to malformations in uterine arterial structure and function following high altitude gestation is an active area of investigation. This work was supported by the National Institutes of Health Grants NIH R01HL155295, R01HL149608, R03HD098477, P01HD083132, and U24DK097154. Additional support was provided by the Loma Linda University School of Medicine and West Coast Metabolomics Center. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Oxygen in the neonatal ICU: a complicated history and where are we now?

Despite major advances in neonatal care, oxygen remains the most commonly used medication in the neonatal intensive care unit (NICU). Supplemental oxygen can be life-saving for term and preterm neonates in the resuscitation period and beyond, however use of oxygen in the neonatal period must be judicious as there can be toxic effects. Newborns experience substantial hemodynamic changes at birth, rapid energy consumption, and decreased antioxidant capacity, which requires a delicate balance of sufficient oxygen while mitigating reactive oxygen species causing oxidative stress. In this review, we will discuss the physiology of neonates in relation to hypoxia and hyperoxic injury, the history of supplemental oxygen in the delivery room and beyond, supporting clinical research guiding trends for oxygen therapy in neonatal care, current practices, and future directions.

Anthocyanins from blueberry ameliorated arsenic-induced memory impairment, oxidative stress, and mitochondrial-biosynthesis imbalance in rat hippocampal neurons

In this study, blueberry anthocyanins extract (BAE) was used to investigate its protective effect on arsenic-induced rat hippocampal neurons damage. Arsenic exposure resulted in elevated levels of oxidative stress, decreased antioxidant capacity and increased apoptosis in rat hippocampal brain tissue and mitochondria. Immunohistochemical results showed that arsenic exposure also significantly decreased the expression of mitochondrial biosynthesis-related factors PGC-1α and TFAM. Treatment with BAE alleviated the decrease in antioxidant capacity, mitochondrial biogenesis related protein PGC-1α/NRF2/TFAM expression, and ATP production of arsenic induced hippocampal neurons in rats, and improved cognitive function in arsenic damaged rats. This study provides new insights into the detoxification effect of anthocyanins on the nervous system toxicity caused by metal exposure in the environment, indicating that anthocyanins may be a natural antioxidant against the nervous system toxicity caused by environmental metal exposure.

Exogenous application of gibberellic acid reduces antioxidant capacity of leaves, resulting in increased Tipburn damages in Lisianthus cultivars

Tipburn (calcium (Ca) deficiency disorder of new leaf tips) is a severe problem in horticultural crop production. Studies have focused on the fact that tipburn commonly occurs during bolting and shown that plants exhibited greater tipburn damage than the control when bolting was induced using exogenous gibberellic acid (GA). However, why exogenous GA application enhances tipburn damage and why tipburn occurs during bolting remains unclear. To address this knowledge gap, we investigated the occurrence of tipburn, Ca concentrations in each organ, antioxidant capacity (superoxide dismutase (SOD) and catalase activity), and gene expression in three lisianthus cultivars (‘Umihonoka’ (UH), ‘Reina White’ (RW), and ‘Voyage Peach’ (VP)), where bolting was induced through exogenous active GA application (GA treatment) and discussed the cause of tipburn occurring during bolting. The incidence and severity of tipburn in the GA treatment were significantly higher than those in the control group in all cultivars. The Ca concentrations in the top leaves of the GA treatment were similar to or higher than those in the control treatment for all cultivars. In contrast, SOD activity in VP was significantly lower in GA treatment than that in the control, which was consistent with the results of SOD-CuZn expression. Additionally, significantly lower catalase activity at GA treatment were detected in the UH and RW than at the control. Recent studies have reported that reactive oxygen species and antioxidants significantly affect the appearance of blossom-end rot. Therefore, exogenous GA application decreased the antioxidant capacity of the upper leaves, resulting in increased tipburn damage. In addition, it is known that a decrease in antioxidant capacity and an increase in H2O2 concentration in leaves of Arabidopsis is a trigger for the initiation of bolting. Our findings provide important insight into the causes and ecological implications of tipburn during bolting.

Neuro-modulatory impact of felodipine against experimentally-induced Parkinson's disease: Possible contribution of PINK1-Parkin mitophagy pathway

Parkinson's disease (PD) is a prevalent neurodegenerative disorder, characterized by motor and psychological dysfunction. Palliative treatment and dopamine replenishment therapy are the only available therapeutic options. Calcium channel blockers (CCBs) have been reported to protect against several neurodegenerative disorders. The current study was designed to evaluate the neuroprotective impact of Felodipine (10 mg/kg, orally) as a CCB on motor and biochemical dysfunction associated with experimentally induced PD using rotenone (2.5 mg/kg, IP) and to investigate the underlying mechanisms. Rotenone induced deleterious neuromotor outcomes, typical of those associated with PD. The striatum revealed increased oxidative burden and NO levels with decreased antioxidant capacity. Nrf2 content significantly decreased with the accumulation of α-synuclein and tau proteins in both the substantia nigra and striatum. These observations significantly improved with felodipine treatment. Of note, felodipine increased dopamine levels in the substantia nigra and striatum as confirmed by the suppression of inflammation and the significant reduction in striatal NF-κB and TNF-α contents. Moreover, felodipine enhanced mitophagy, as confirmed by a significant increase in mitochondrial Parkin and suppression of LC3a/b and SQSTM1/p62. In conclusion, felodipine restored dopamine synthesis, attenuated oxidative stress, inflammation, and mitochondrial dysfunction, and improved the mitophagy process resulting in improved PD-associated motor impairment.

Effect of UV Stress on the Antioxidant Capacity, Photosynthetic Activity, Flavonoid and Steviol Glycoside Accumulation of Stevia rebaudiana Bertoni

Lighting conditions are an important controller of plant growth and development, and they affect secondary metabolite synthesis. In this research, we explored the effect of additional UV irradiation of various ranges in addition to the main one at PPFD 160 µmol m−2 s−1 on the accumulation of some secondary metabolites of stevia (Stevia rebaudiana Bertoni). The fresh weight of leaves was slightly higher under additional UV-A and UV-B irradiation compared with the control variant, and the leaf surface area was significantly larger, respectively, by 23.3 and 20.7% than in the control variant, while the rate of photosynthesis did not decrease. Plants under additional UV-B and UV-C irradiation were under the greatest light stress, as evidenced by a decrease in antioxidant capacity by an average of 30% compared to the control and UV-A. The total flavonoid content was significantly higher (by 74%) under UV-B irradiation. The highest concentration of steviol glycoside was observed during budding and flowering under UV-B and UV-C irradiation (by 13.2 and 11.3%, respectively). Analysis of hyperspectral images, chlorophyll fluorescence, and vegetation indices showed light stress increasing under UV-C irradiation, which caused an increase in the relative chlorophyll content, scorches, leaf morphology changes, a CO2 absorption rate decrease, and plant growth inhibition. UV-B irradiation can be used as an optimal type of irradiation based on a set of indicators.

Impact of Heavy Metals on Cold Acclimation of Salix viminalis Roots.

In nature, plants are exposed to a range of climatic conditions. Those negatively impacting plant growth and survival are called abiotic stresses. Although abiotic stresses have been extensively studied separately, little is known about their interactions. Here, we investigate the impact of long-term mild metal exposure on the cold acclimation of Salix viminalis roots using physiological, transcriptomic, and proteomic approaches. We found that, while metal exposure significantly affected plant morphology and physiology, it did not impede cold acclimation. Cold acclimation alone increased glutathione content and glutathione reductase activity. It also resulted in the increase in transcripts and proteins belonging to the heat-shock proteins and related to the energy metabolism. Exposure to metals decreased antioxidant capacity but increased catalase and superoxide dismutase activity. It also resulted in the overexpression of transcripts and proteins related to metal homeostasis, protein folding, and the antioxidant machinery. The simultaneous exposure to both stressors resulted in effects that were not the simple addition of the effects of both stressors taken separately. At the antioxidant level, the response to both stressors was like the response to metals alone. While this should have led to a reduction of frost tolerance, this was not observed. The impact of the simultaneous exposure to metals and cold acclimation on the transcriptome was unique, while at the proteomic level the cold acclimation component seemed to be dominant. Some genes and proteins displayed positive interaction patterns. These genes and proteins were related to the mitigation and reparation of oxidative damage, sugar catabolism, and the production of lignans, trehalose, and raffinose. Interestingly, none of these genes and proteins belonged to the traditional ROS homeostasis system. These results highlight the importance of the under-studied role of lignans and the ROS damage repair and removal system in plants simultaneously exposed to multiple stressors.

Exploitation of the biocontrol potential of a marine-derived Bacillus velezensis and its application on postharvest strawberry

Fresh strawberry fruits have a significant postharvest diseases incidence and economical losses. To explore more effective postharvest management instruments, a strain of Bacillus velezensis 12Y with excellent antagonistic activity was isolated from the Nanhai Sea. Its whole genome and activity against fruit fungal pathogens was studied. The genomic sequencing revealed that 12Y contains an abundance of functional gene related to biocontrol and biosynthetic gene clusters of secondary metabolites with potential antimicrobial properties. In the strawberry preservation experiment, 12Y fermentation broth (YFB) could effectively reduce the natural decay and extend shelf life of strawberry by delaying the decline of total soluble solids and titratable acid with no adverse effects on weight loss and hardness. Moreover, YFB could enhance the activity of key enzymes in phenylpropanoid metabolism pathway, induce the accumulation of anthocyanin and total phenols, delay the decrease of antioxidant capacity, and reduce the peroxidation of strawberry cell membranes. This study demonstrated the potential of B. velezensis 12Y as an excellent biocontrol bacteria and a promising preservation agent for strawberry.

Chemical Composition, Functional and Antioxidant Properties of Dietary Fibre Extracted from Lemon Peel after Enzymatic Treatment.

Lemon peel represents an interesting by-product owing to its content of dietary fibre (DF) and (poly)phenols, which is of great importance for its valorisation. Hence, the objective of this study was to characterise the DF, total phenolic content (TPC), and antioxidant capacity of two lemon-peel-derived ingredients using two different methods (drying with warm air and enzymatic hydrolysis with pectinesterase). The analysis included a DF assessment, followed by neutral sugars characterisation through GC-FID and uronic acids determination via colorimetry. Subsequently, TPC and antioxidant capacity using the FRAP method were quantified through spectrophotometry. The swelling capacity (SWC), water retention capacity (WRC), and fat absorption capacity (FAC) were also determined as functional properties. It was observed that pectinesterase treatment led to a reduction in soluble DF and an increase in insoluble DF. This treatment also affected the pectin structure, thereby diminishing its ability to absorb water and fat within its matrix. The TPC was also reduced, resulting in a decrease in antioxidant capacity. Conversely, employing warm air exhibited a noteworthy increase in antioxidant capacity. This underscores its crucial contribution to the valorisation of lemon peel, not only by diminishing the environmental impact but also by enabling the acquisition of fibre ingredients with a noteworthy antioxidant capacity.

2,4-D Herbicide-Induced Hepatotoxicity: Unveiling Disrupted Liver Functions and Associated Biomarkers.

2,4-dichlorophenoxyacetic acid (2,4-D) is a widely used herbicide worldwide and is frequently found in water samples. This knowledge has prompted studies on its effects on non-target organisms, revealing significant alterations to liver structure and function. In this review, we evaluated the literature on the hepatotoxicity of 2,4-D, focusing on morphological damages, toxicity biomarkers and affected liver functions. Searches were conducted on PubMed, Web of Science and Scopus and 83 articles were selected after curation. Among these studies, 72% used in vivo models and 30% used in vitro models. Additionally, 48% used the active ingredient, and 35% used commercial formulations in exposure experiments. The most affected biomarkers were related to a decrease in antioxidant capacity through alterations in the activities of catalase, superoxide dismutase and the levels of malondialdehyde. Changes in energy metabolism, lipids, liver function, and xenobiotic metabolism were also identified. Furthermore, studies about the effects of 2,4-D in mixtures with other pesticides were found, as well as hepatoprotection trials. The reviewed data indicate the essential role of reduction in antioxidant capacity and oxidative stress in 2,4-D-induced hepatotoxicity. However, the mechanism of action of the herbicide is still not fully understood and further research in this area is necessary.

Increased NAD+ levels protect female mouse reproductive system against zearalenone-impaired glycolysis, lipid metabolism, antioxidant capacity and inflammation

The reproductive system is a primary target organ for zearalenone (ZEN, a widespread fusarium mycotoxin) to exert its toxic effects, including decreased antioxidant capacity and aggravated inflammatory response. These ZEN-induced reproductive abnormalities are partially caused by the declining levels of nicotinamide adenine dinucleotide (NAD+), which results in an imbalance in lipid/glucose metabolism. Accordingly, the present study aimed to investigate whether supplements of nicotinamide mononucleotide (NMN, a NAD+ precursor) in female mice could protect against ZEN-induced reproductive toxicity. In this study, thirty female mice were randomly divided into three groups that were intragastrically administered with i) 0.5% DMSO (the Ctrl group), ii) 3 mg/(kg bw.d) ZEN (the ZEN group), or iii) ZEN + 500 mg/(kg bw.d) NMN (the ZEN/NMN group) for two weeks. The results revealed that, compared with the Ctrl group, animals exposed to ZEN exhibited reproductive toxicity, such as decreased antioxidant capacity and aggravated inflammatory response in reproductive tissues. These effects were strongly correlated with lower activities in key glycolytic enzymes (e.g., ALDOA and PGK), but increased expressions in key lipid-synthesis genes (e.g., LPIN1 and ATGL). These changes contribute to lipid accumulation, specifically for diacylglycerols (DAGs). Furthermore, these ZEN-induced changes were linked with disturbed NAD+ synthesis/degradation, and subsequently decreased NAD+ levels. Notably, NMN supplements in mice protected against these ZEN-induced reproductive abnormalities by boosting NAD+ levels. Herein, the present findings demonstrate that potential strategies to enhance NAD+ levels can protect against ZEN-induced reproductive toxicity.

Oxidative Stress and Glycaemic Control in Type 2 Diabetes Mellitus

Introduction: There is growing evidence that excess generation of highly reactive free radicals largely due to hyperglycaemia cause oxidative stress which further exacerbates the development and progression of type 2 diabetes mellitus and its complications. Objective: This study aims to assess glycaemic status and oxidative stress in type 2 diabetes mellitus patients. Methods: Forty confirmed Type 2 diabetes mellitus patients registered with the General Medicine department of Mamata General Hospital, Khammam, Andhra Pradesh were selected for the study. Based on HbA1 c levels these patients were subdivided into two groups one with HbA1 c levels >8.5% was considered poor glycaemic control and the other with HbA1 c levels ≤8.5% was considered as good glycaemic control. Malondialdehyde and total antioxidant capacity were measured among the cases and controls. Results: This study reveals the comparison of glycated haemoglobin, malondialdehyde, and total antioxidant capacity in 40 confirmed cases of Type 2 Diabetes Mellitus, which included 19 good glycaemic control and 21 poor glycaemic control. Firstly, the comparison of HbA1C (P value: 0.01), MDA (P value: 0.02) and TAC (P value: 0.04) revealed the significant difference between good glycaemic control and poor glycaemic control. Moreover, the Pearson correlation revealed a significant positive correlation of HbA1C with MDA (+0.72, 0.02) and a negative correlation with TAC (-0.01, 0.7) which was not statistically significant. Conclusions: It is observed that poor glycaemic control has resulted in increased oxidative stress and decreased antioxidant capacity which can ultimately lead to complications. Antioxidant supplementation may help the patients in overall improvement and may delay the complications.

The interplay of oxidative stress and inflammation in pediatric patients with nephrotic syndrome

Summary 
 Background: The pathophysiological mechanisms crucial in the development of nephrotic syndrome (NS) in the pediatric population are still not fully understood. This study aims to investigate the synergistic interaction of oxidative stress and inflammation in the pathogenesis of NS. Additionally, one of the objectives of this study is to examine the relationship between hypertension and the degree of oxidative stress and inflammation in patients during the acute phase of the disease. 
 Methods: The study included 33 children, aged 2 to 9 years, with NS. Blood samples were collected during the acute phase and remission. Parameters of oxidative status were determined, including total oxidative status (TOS), advanced oxidation protein products (AOPP), prooxidant-antioxidant balance (PAB), sulfhydryl groups (-SH), paraoxonase 1 (PON1), and total antioxidant status (TAS) in serum, measured spectrophotometrically. Inflammatory parameters such as pentraxin 3 (PTX3), leptin, programmed cell death ligand 1 (PD-L1), and E-cadherin were determined using enzyme-linked immunosorbent assay (ELISA).
 Results: Patients with NS and hypertension had significantly higher levels of AOPP and TOS (p=0.029 and p=0.003, respectively). During the acute phase of the disease, lower activity of -SH and PON1 was observed compared to remission (p<0.001, for both). PTX3 levels were higher, while leptin levels were lower during the acute phase (p<0.001, for both). PTX3 correlated with AOPP and TAS during the acute phase but not in remission (rs=0.42, p=0.027 and rs=0.43, p=0.025, respectively). A negative correlation between AOPP and leptin was observed during the acute phase, which disappeared in remission (rs=-0.42, p=0.028).
 
 Conclusions: Results of this study show that hypertension influences oxidative stress markers, and decreased antioxidant capacity may contribute to NS development. PTX 3 appears as a potential disease activity marker, indicating a dynamic connection between inflammation and oxidative stress. Leptin may also play a role in oxidative stress in NS. 
 List of abbreviations: AOPP, advanced oxidation protein products; BMI, body mass index; DBP, diastolic blood pressure; ELISA, enzyme-linked immunosorbent assay; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; total antioxidant status; PAB, prooxidant-antioxidant balance; -SH, sulfhydryl group; SBP, systolic blood pressure; PON 1, paraoxonase; PTX 3, pentraxin 3; PD-L1, programmed cell death ligand 1; TC, total cholesterol; TG, triglyceride; TAS, total antioxidant status; TOS, total oxidation status.

Modulation of gene expression and influence of gene polymorphisms related to genotoxicity and redox status on occupational exposure to inhaled anesthetics

The extensive use of inhalational anesthetics contributes to both indoor and outdoor (environmental) pollution. The influence of genetic susceptibility on DNA damage and oxidative stress and the possible modulation of gene expression have not yet been investigated upon occupational exposure to waste anesthetic gases (WAGs). This study assessed 8-oxoguanine DNA glycosylase 1 (OGG1) and superoxide dismutase 2 (SOD2) gene expression, which are related to oxidized DNA repair and antioxidant capacity, respectively, and the influence of their polymorphisms (OGG1 rs1052133 and SOD2 rs4880) in 100 professionals highly exposed to WAGs and 93 unexposed volunteers (control group). Additionally, X-ray repair cross complementing 1 (XRCC1 rs25487 and rs1799782) and ataxia telangiectasia mutated (ATM rs600931) gene polymorphisms as well as genetic instability (micronucleus-MN and nuclear bud-NBUD) and oxidative stress (malondialdehyde-MDA and ferric reducing antioxidant power-FRAP) biomarkers were assessed in the groups (control and exposed) and in the subgroups of the exposed group according to job occupation (anesthesiologists versus surgeons/technicians). Except for the ATM TT controls (associated with increased FRAP), there were no influences of OGG1, XRCC1, ATM, and SOD2 polymorphisms on MN, NBUD, MDA, and FRAP values in exposed or control subjects. No significant difference in the expression of either gene evaluated (OGG1 and SOD2) was found between the exposed and control groups. Increased OGG1 expression was observed among OGG1 -/Cys individuals only in the control group. Among the exposed group, anesthesiologists had a greater duration of WAG exposure (both h/week and years) than surgeons/technicians, which was associated with increased MDA and decreased antioxidant capacity (FRAP) and SOD2 expression (redox status). Higher expression of OGG1 was found in -/Cys surgeons/technicians than in anesthesiologists with the same genotype. Increased antioxidant capacity was noted in the surgeons/technicians carrying the ATM T allele and in those carrying XRCC1 -/Gln. Increased MN was influenced by OGG1 -/Cys in surgeons/technicians. Anesthesiologists with ATM CC exhibited increased MN, and those carrying the C allele (CC/CT genotype) exhibited increased NBUD. SOD2 polymorphism did not seem to be relevant for WAG exposure. These findings contribute to advancing the knowledge on genetic susceptibility/gene expression/genetic instability/oxidative stress, including differences in job occupation considering the workload, in response to occupational exposure to WAGs.

Supplementation with Manihot esculenta Crantz (Cassava) leaves’ extract prevents recognition memory deficits and hippocampal antioxidant dysfunction induced by Amyloid-β

ABSTRACT Objective: The Manihot esculenta Crantz (Cassava) is a typical South American plant rich in nutrients and energetic compounds. Lately, our group has shown that non-pharmacological interventions with natural antioxidants present different neuroprotective effects on oxidative balance and memory deficits in AD-like animal models. Here, our objective was to evaluate the neuroprotective effects of Cassava leaves’ extract (CAS) in an AD-like model induced by amyloid-beta (Aβ) 25–35 peptide. Methods: Male Wistar rats (n = 40; 60 days old) were subjected to 10 days of CAS supplementation; then, we injected 2 μL Aβ 25–35 in the hippocampus by stereotaxic surgery. Ten days later, we evaluated object recognition (OR) memory. Cassavas’ total polyphenols, flavonoids, and condensed tannins content were measured, as well as hippocampal lipid peroxidation and total antioxidant capacity. Results: CAS protected against Aβ-induced OR memory deficits. In addition, Aβ promoted antioxidant capacity decrease, while CAS was able to prevent it, in addition to diminishing lipoperoxidation compared to Aβ. Discussion: We show that treatment with Cassava leaves’ extract before AD induction prevents recognition memory deficits related to Aβ hippocampal injection. At least part of these effects can be related to the Cassava leaves’ extract supplementation effects on diminishing lipid peroxidation and preventing a decrease in the hippocampal total antioxidant capacity in the hippocampus of AD-like animals without adverse effects. Once cassavais a plant of warm and dry ground that can adapt to growon various soil types and seems to resist several insects, our results enable Cassava to be considered asa potential preventive intervention to avoid or minimizeAD-induced memory deficits worldwide.

Fabrication, spectroscopic properties, antioxidant and antimicrobial activities of Chitosan-CaLi@Flumox nanocomposites

In the current study, we examined the impact of introducing Flumox into the chitosan/calcium lithium (Chitosan-CaLi) nanocomposite on its spectroscopic, thermal, and antimicrobial characteristics. The formation of the nanocomposites was achieved using the sol–gel method/polymerization, which was chosen for its cost-effectiveness and straightforward processing. The UV–Visible optical analysis shows an absorption peak at 290 nm across all samples. Both direct and indirect energy gap types are available where the indirect event exhibits a higher value than the direct transition. There is a noticeable decrease in both transition energies with the increase in Flumox content. The findings indicated that as the Flumox concentration increased, the Ic50 value also increased, signifying a decrease in antioxidant capacity. The results from the obtained systems revealed that chitosan-CaLiO nanoparticles loaded with Flumox exhibited remarkable antimicrobial activity, particularly against Pseudomonas aeruginosa and Staphylococcus aureus, demonstrating the highest growth inhibition rate. However, in the case of Aspergillus niger and Candida albicans, the antimicrobial activity was comparatively lower.

α-Pyrrolidinononanophenone derivatives induce differentiated SH-SY5Y neuroblastoma cell apoptosis via reduction of antioxidant capacity: Involvement of NO depletion and inactivation of Nrf2/HO1 signaling pathway

α-Pyrrolidinononanophenone (α-PNP) derivatives are known to be one of the hazardous new psychoactive substances due to the most extended hydrocarbon chains of any pyrrolidinophenones on the illicit drug market. Our previous report showed that 4'-iodo-α-PNP (I-α-PNP) is the most potent cytotoxic compound among α-PNP derivatives and induces apoptosis due to mitochondrial dysfunction and suppression of nitric oxide (NO) production in differentiated human neuronal SH-SY5Y cells. In this study, to clarify the detailed action mechanisms by I-α-PNP, we investigated the mechanism of reactive oxygen species (ROS) -dependent apoptosis by I-α-PNP in differentiated SH-SY5Y with a focus on the antioxidant activities. Treatment with I-α-PNP elicits overproduction of ROS such as H2O2, hydroxyl radical, and 4-hydroxy-2-nonenal, and pretreatment with antioxidant N-acetyl-L-cysteine is attenuated the SH-SY5Y cells apoptosis by I-α-PNP. These results suggested that the overproduction of ROS is related to SH-SY5Y cell apoptosis by I-α-PNP. In addition, I-α-PNP markedly decreased antioxidant capacity in differentiated cells than in undifferentiated cells and inhibited the upregulation of hemeoxygenase 1 (HO1) and glutathione peroxidase 4 (GPX4) expression caused by induction of differentiation. Furthermore, the treatment with I-α-PNP increased the nuclear expression level of BTB Domain And CNC Homolog 1 (Bach1), a transcriptional repressor of Nrf2, only in differentiated cells, suggesting that the marked decrease in antioxidant capacity in differentiated cells was due to suppression of Nrf2/HO1 signaling by Bach1. Additionally, pretreatment with an NO donor suppresses the I-α-PNP-evoked ROS overproduction, HO1 down-regulation, increased nuclear Bach1 expression and reduced antioxidant activity in the differentiated cells. These findings suggest that the ROS-dependent apoptosis by I-α-PNP in differentiated cells is attributed to the inactivation of the Nrf2/HO1 signaling pathway triggered by NO depletion.

Gentisic acid ameliorates cisplatin-induced reprotoxicity through suppressing endoplasmic reticulum stress and upregulating Nrf2 pathway

Reproductive toxicity is a serious side effect of cisplatin (CP) chemotherapy. Gentisic acid (GTA) is a phenolic acid with strong antioxidant properties. Here, we aimed to determine therapeutic effect of GTA against CP-induced testicular toxicity in rats for the first time. Male Sprague-Dawley rats received a single dose of CP (5 mg/kg; intraperitoneal) and treated with GTA (1.5 and 3 mg/kg; intraperitoneal; 3 consecutive days). The levels of oxidative stress (OS), inflammation, endoplasmic reticulum stress (ERS) and apoptosis biomarkers were assessed in the testicular tissue of rats. In addition, how CP affects the nuclear factor erythroid-2-related factor 2 (Nrf2) pathway and the effect of GTA on this situation were also addressed in the testicular tissue. CP administration induced histopathological changes in testicular tissue of rats with a significant increase in OS, inflammation, ERS and apoptosis biomarkers and a decrease in antioxidant capacity and Nrf2 expression levels. Administrations of GTA resulted in an amelioration of these altered parameters. These data suggest that GTA may be a potential therapeutic agent against CP-induced testicular toxicity. Activation of the Nrf2 pathway plays a key role of this therapeutic effect of GTA.