Decreased Antioxidant Enzyme Research Articles

Superoxide dismutase and glutathione peroxidase content in children with type 1 diabetes mellitus

Type 1 diabetes mellitus (T1D) is one of the most frequently diagnosed chronic diseases of childhood. Oxidative stress (OS) is considered as one of the possible mechanisms of its development and complications. The aim of the study was to analyze the content of the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GP) in children and adolescents with adequately controlled T1D.Material and methods. A total of 58 children were examined, including 34 children with type 1 diabetes (study group) and 24 conditionally healthy children (control group). The content of glycated hemoglobin, blood plasma glucose per day, post-prandial glucose, total protein, creatinine and urea were determined by conventional methods, as well as the level of SOD and GP in the blood serum by ELISA.Results and discussion. A significant decrease in the content of both enzymes was found in type 1 DM patients compared to conditionally healthy children. In patients with the chronic form of the disease, SOD and GP level was significantly lower than in patients with incident T1D. An inverse correlation was revealed between the antioxidant enzymes level on the one hand and age, duration of the disease, and the number of episodes with a poor glucose history on the other hand. The decrease in SOD and GP concentration was associated with an increase in glycated hemoglobin and plasma glucose level over a 24-hour period in patients with chronic type SD 1. The decrease in SOD concentrations was associated with an increase in glycated hemoglobin in patients with T1D chronic type. The discovered abnormalities indicate that decreased antioxidant enzyme level represent a manifestation of OS in patients with adequately controlled type 1 DM.Conclusions. Content of antioxidant enzymes in children with T1D provides an important criterion for the assessment of OS manifestations in this disease.

Protective effects of sinapic acid against lead acetate-induced nephrotoxicity: a multi-biomarker approach.

Lead acetate (PbAc) is one of the top five most dangerous toxic heavy metals, particularly leading to kidney damage and posing serious health risks in both humans and animals. Sinapic acid (SNP) is a naturally occurring flavonoid found in fruits and vegetables that stands out with its antioxidant, anti-inflammatory, and anticancer properties. This is the first study to investigate the effects of SNP on oxidative stress, inflammation, apoptosis, autophagy and endoplasmic reticulum (ER) stress in PbAc-induced nephrotoxicity in rats by biochemical, molecular and histological methods. 35 Spraque dawley rats were randomly divided into five groups of 7 rats each: control, PbAc, SNP (10mg/kg), PbAc + SNP 5, PbAC + SNP 10. PbAc at a dose of 30 mg/kg body weight was administered via oral gavage alone or in combination with SNP (5 and 10 mg/kg body weight) via oral gavage for seven days. While PbAc impaired renal function by increasing serum urea and creatinine levels, SNP decreased these levels and contributed to the improvement in renal function. The administration of SNP reduced oxidative stress by increasing PbAc-induced decreased antioxidant enzyme (SOD, CAT, and GPx) activities and GSH levels, decreasing MDA levels, a marker of increased lipid peroxidation. SNP administration reduced NF-κB, TNF-α, IL-1β, NLRP3, and RAGE mRNA transcription levels, NF-κB, and TNF-α protein levels that are among the PbAc-induced increased inflammation parameters. Decreases in antiapoptotic Bcl-2 and increases in apoptotic Bax, APAF-1, and Caspase-3 due to PbAc exposure, SNP reversed the situation. SNP reduced ER stress caused by PbAc by increasing PERK, IRE1, ATF-6, CHOP, and GRP-78 levels and made it tend to regress. SNP reduced autophagy damage by decreasing the Beclin-1 protein level increased by PbAc. The findings of the present study suggested that SNP attenuates PbAc-induced nephrotoxicity.

Protective Effect of Daidzein against Diethylnitrosamine/Carbon Tetrachloride-Induced Hepatocellular Carcinoma in Male Rats.

Hepatocellular carcinoma (HCC) is the second-largest cause of death among all cancer types. Many drugs have been used to treat the disease for a long time but have been mostly discontinued because of their side effects or the development of resistance in the patients with HCC. The administration of DZ orally is a great focus to address the clinical crisis. Daidzein (DZ) is a prominent isoflavone polyphenolic chemical found in soybeans and other leguminous plants. It has various pharmacological effects, including anti-inflammatory, antihemolytic, and antioxidant. This present study investigates the protective effect of DZ on chemically induced HCC in rat models. The DZ was administered orally four weeks before HCC induction and continued during treatment. Our study included four treatment groups: control (group 1, without any treatment), HCC-induced rats (group II), an HCC group treated with DZ at 20 mg/kg (group III), and an HCC group treated with DZ at 40 mg/kg (group IV). HCC rats showed elevation in all the HCC markers (AFP, GPC3, and VEGF), liver function markers (ALP, ALT, and AST), inflammatory markers (IL-6, TNF-α, and CRP), and lipid markers concomitant with a decrease in antioxidant enzymes and protein. However, groups III and IV demonstrated dose-dependent alleviation in the previous parameters resulting from HCC. In addition, the high dose of DZ reduces many hepatological changes in HCC rats. All study parameters improved with DZ administration. Due to its antioxidant and anti-inflammatory characteristics, DZ is a promising HCC treatment option for clinical use.

Evaluation of the Antidiabetic Potentials of Musa acuminata Leaves Crude Extract in Alloxan-Induced Wistar Rats

Context: Musa acuminata is a plant of the tropical and subtropical regions. Over the past few decades, the health benefits of Musa acuminata have received much attention. All parts of the plant, including fruits, peel, pseudo stem, corm, flowers, leaves, sap, and roots, have found their use in treating many diseases in traditional medicine.
 Aim: This study was conducted to appraise the protective effect of Musa acuminata extract on alloxan-induced Diabetics Mellitus in wistar rats.
 Settings and Design: This investigation was carried out using 24 Wistar rats, both males and females. The experimental models were divided into six groups; 4 rats per group.
 Materials and Methods: The experimental models were divided into six groups; 4 rats per group. Alloxan was intraperitonially injected at a dose of 150 mg/kg body weight for day 1 across all groups except the positive control which is Group A together with oral administration of the aqueous extract of Musa acuminata (100 mg/kg, 200mg/kg and 300mg/kg body weight for the treatment group) and Group F was administered a standard drug. The animals were sacrificed on the 11th day under deep anesthesia with chloroform. The blood was collected by cardiac puncture and kidneys were collected for the histological profile.
 Statistical Analysis: Kidney oxidative stress marker Malondialdehyde (MDA) and antioxidant enzyme activities Creatinine and Urea, were determined.
 Results: The alloxan injection indicated an increase in Malondialdehyde (MDA), with a decrease in Urea and Creatinine when compared with the control. A remarkable decrease in antioxidant enzymes was also observed. Oxidant/antioxidant imbalance, alloxan-induced diabetic mellitus, and histological changes in the kidneys were reduced almost to normal by the administration of Musa acuminata.
 Conclusion: Based on the current findings, Musa acuminata leaves at low dose (100 mg/kg body weight) in the alloxan Induced Wistar rat has some anti diabetics potential than at 200 mg/kg body weight, 300 mg/kg body weight and standard drug (Metformin).

Single and Combined Effects of Chlorpyrifos and Glyphosate on the Brain of Common Carp: Based on Biochemical and Molecular Perspective.

Chlorpyrifos (CPF) and glyphosate (GLY) are the most widely used organophosphate insecticide and herbicide worldwide, respectively; co-occurrence of CPF and GLY in aquatic environments occurs where they inevitably have potential hazards to fish. However, the potential mechanisms of CPF and GLY to induce toxicity have not been fully explored. To identify the adverse impacts of CPF and GLY on fish, either alone or in combination (MIX), CPF (25 μg/L) and GLY (3.5 mg/L) were set up according to an environmentally relevant concentration to expose to common carp for 21 days. After exposure, CPF and GLY decreased the activities of acetylcholinesterase and Na+/K+-ATPase, altered monoamine oxidase levels, decreased antioxidant enzyme activities (superoxide dismutase, catalase, glutathione S-transferase and glutamic reductase), and induced the accumulation of malondialdehyde in the carp brain. The parameters in the MIX groups had a greater impact compared to that in the CPF or GLY group, suggesting that both single and combined exposure could affect neurological signaling systems and cause oxidative stress and lipid peroxidation damage in carp brains, and that MIX exposure increases the impact of each pollutant. RNA-seq results showed that single or combined exposure to CPF and GLY induced global transcriptomic changes in fish brains, and the number of differentially expressed genes in MIX-treated carp brains were globally increased compared to either the CPF or GLY groups, suggesting that the effects of co-exposure were greater than single exposure. Further analysis results revealed that the global transcriptomic changes participated in oxidative stress, immune dysfunction, and apoptosis of fish brains, and identified that the P13k-Akt signaling pathway participates in both single and combined exposure of CPF- and GLY-induced toxicity. Taken together, our results demonstrated that the interaction of CPF and GLY might be synergic and provided novel insights into the molecular mechanisms of fish brains coping with CPF and GLY.

Protective effect of grape seed extract and exercise training on tissues toxicities in doxorubicin-treated healthy rat

Objective The aim of the present study was to investigate the effects of Grape seed extract (GSE) and exercise training on Doxorubicin (Doxo)-induced cardio, hepato and myo toxicities in healthy rats. Methods Thirty male Wistar rats were randomly divided into five groups and daily treated by intraperitoneal route during two months either with ethanol 10% (Control); Doxo (1.5 mg/kg); Doxo + exercise (1.5 mg/kg + swimming exercise for 30 min twice a week); Doxo + GSE (1.5 mg/kg + GSE 2.5 g/kg); Doxo + GSE + exercise (1.5 mg/kg + GSE 2.5 g/kg + swimming exercise for 30 min twice a week). At the end of the treatment, tissues were collected and processed for the determination of oxidative stress (OS), intracellular mediators, energy fuelling biomarkers, carbohydrate metabolism parameters and muscle histopathology. Results Doxo provoked OS characterised by an increased lipoperoxidation (LPO) and protein carbonylation and decreased antioxidant enzyme activities. Doxo also affected intracellular mediators, disturbed carbohydrate metabolism and energy fuelling in skeletal muscle as assessed by down-regulated Electron Transport Chain (ETC) complex activities leading in fine to altered skeletal muscle structure and function. Conclusion Almost all Doxo-induced disturbances were partially corrected with GSE and exercise on their own and more efficiently with the combined treatment (GSE + exercise).

The protective effect of forsythiaside A on 3,5-diethoxycarbonyl-1,4-dihydrocollidine-induced cholestatic liver injury in mice: Based on targeted metabolomics and molecular biology technology

Cholestasis is a disorder of bile secretion and excretion caused by a variety of etiologies. At present, there is a lack of functional foods or drugs that can be used for intervention. Forsythiaside A (FTA) is a natural phytochemical component isolated from the medicinal plant Forsythia suspensa (Thunb.) Vahl, which has a significant hepatoprotective effect. In this study, we investigated whether FTA could alleviate liver injury induced by cholestasis. In vitro, FTA reversed the decrease in viability of human intrahepatic bile duct epithelial cells, the decrease in antioxidant enzymes (SOD1, CAT and GSH-Px), and cell apoptosis induced by lithocholic acid. In vivo, FTA protected mice from 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-induced liver injury, abnormal serum biochemical indexes, abnormal bile duct hyperplasia, and inflammatory infiltration. Furthermore, FTA treatment alleviated liver fibrosis by inhibiting collagen deposition and HSC activation. The metabonomic results showed that DDC-induced bile acid disorders in the liver and serum were reversed after FTA treatment, which may benefit from the activation of the FXR/BSEP axis. In addition, FTA treatment increased the levels of antioxidant enzymes in the serum and liver. Meanwhile, FTA treatment inhibited ROS and MDA levels and cleaved caspase 3 protein expression, thereby reducing DDC-induced hepatic oxidative stress and apoptosis. Further studies showed that the antioxidant effects of FTA were dependent on the activation of the BRG1/NRF2/HO-1 axis. In a word, FTA has a significant hepatoprotective effect on cholestatic liver injury, and can be further developed as a functional food or drug to prevent and treat cholestatic liver injury.

Melatonin improves oxidative state and lactate metabolism in rodent Sertoli cells

Antioxidant actions of melatonin and its impact on testicular function and fertility have already been described. Considering that Sertoli cells contribute to provide structural support and nutrition to germ cells, we evaluated the effect of melatonin on oxidative state and lactate metabolism in the immature murine TM4 cell line and in immature hamster Sertoli cells.A prooxidant stimulus applied to rodent Sertoli cells expressing MT1/MT2 receptors, increased lipid peroxidation whereas decreased antioxidant enzymes (superoxide dismutase 1, catalase, peroxiredoxin 1) expression and catalase activity. These changes were prevented by melatonin. Furthermore, melatonin stimulated lactate dehydrogenase (LDH) expression/activity via melatonin receptors, and increased intracellular lactate production in rodent Sertoli cells.Interestingly, oral melatonin supplementation in infertile men positively regulated LDHA testicular mRNA expression.Overall, our work provides insights into the potential benefits of melatonin on Sertoli cells contributing to testicular development and the future establishment of a sustainable spermatogenesis.

Earthworm activity effectively mitigated the negative impact of microplastics on maize growth

Microplastic pollution can have detrimental effects on soil environments and inhibit crop growth. Earthworms, known as soil engineers, promote crop growth, but their role and impact on the amelioration of microplastic-polluted soil is not yet clear. In this study, we investigated the impact and pathways of earthworm activity on microplastic-contaminated soil by introducing varying densities (without earthworm:0, low-density: 1, medium-density: 2, high-density: 5 ind column−1) of earthworms (epi-endogeic) into soil contaminated with two types of microplastics: polyethylene and polyvinyl chloride. Our results showed that earthworms all survived in soil polluted with two types of microplastics. Meanwhile, earthworm activity increased nutrient content and enzyme activity by 0.2–36.1% and 2.9–34.3%, respectively, and significantly increased soil microbial biomass and community diversity index. Earthworm activity also decreased antioxidant enzyme activity and promoted maize plant growth, including agronomic traits such as plant height, biomass, root length, and root surface area. Furthermore, the nutrient content of maize organs increased by 1.1–29.7%. Partial least squares models confirmed that earthworm activity alleviated the stress effect of microplastic pollution on plant growth by improving soil structure, fertility, and microbial abundance and diversity. The greatest effect on maize growth was observed with the improvement of soil physical-chemical properties. Our results suggest that medium densities of earthworms have the greatest soil improvement effect and provide an important basis for bioremediation of farmland contaminated by microplastics and promoting green and efficient development in agriculture.

Comparative Effect of Chemical and Green Zinc Nanoparticles on the Growth, Hematology, Serum Biochemical, Antioxidant Parameters, and Immunity in Serum and Mucus of Goldfish, Carassius auratus (Linnaeus, 1758).

Recently, nano feed supplement research has great attention to improving healthy aquatic production and improving the aquatic environment. With the aims of the present study, chemical and green synthesized nanoparticles are characterized by various instrumentation analyses, namely UV-Vis spectrophotometry (UV-Vis), X-ray diffraction (XRD), Fourier transform infra-red (FTIR) spectroscopy, and scanning electron microscope (SEM). After characterization analysis of these nanoparticles utilized in aquatic animals, the composition ratio is as follows: controls (without ZnO-NPs (0 mg/L)), T1 (0.9 mg/L ZnO-NPs), T2 (1.9 mg/L ZnO-NPs), T3 (0.9 mg/L GZnO-NPs), T4 (1.9 mg/L GZnO-NPs). SEM investigation report demonstrates that the structure of the surface of green synthesized zinc oxide nanoparticles (GZnO-NPs) was conical shape and the size ranging was from 60 to 70 nm. Concerning hematological parameters, the quantity of hemoglobin increased in different doses of green zinc nanoparticles, but the values of MCV and MCH decreased somewhat. However, this decrease was the highest in the T2 group. Total protein and albumin decreased in T2 and triglyceride, cholesterol, glucose, cortisol, creatinine, and urea increased, while in T3 and T4 groups, changes in biochemical parameters were evaluated as positive. Mucosal and serum immunological parameters in the T2 group showed a significant decrease compared to other groups. In zinc nanoparticles, with increasing dose, oxidative damage is aggravated, so in the T2 group, a decrease in antioxidant enzymes and an increase in MDA were seen compared to other groups. In this regard, the concentration of liver enzymes AST and ALT increased in the T2 group compared with control and other groups. This can confirm liver damage in this dose compared with control and other groups. This research work suggests that green synthesized form of zinc nanoparticles in higher doses have less toxic effectsin comparison to the chemical form of zinc nanoparticles and can act as suitable nutrient supplements in aquatic animals.

Difenoconazole disrupts carp intestinal physical barrier and causes inflammatory response via triggering oxidative stress and apoptosis

As a common fungicide, difenoconazole (DFZ) is widespread in the natural environment and poses many potential threats. Carp makes up a significant proportion of China's freshwater aquaculture population and are vulnerable to the DFZ. Therefore, this study investigated the effects of DFZ (0.488 mg/L and 1.953 mg/L) exposure for 4 d on the intestinal tissues of carp and explored the mechanisms. Specifically, DFZ exposure caused pathological damage to the intestinal tissues of carp, reducing the expression levels of intestinal tight junction proteins, and leading to damage to the intestinal barrier. In addition, DFZ exposure activated the NF-κB signaling pathway, increasing the levels of pro-inflammatory factors (TNF-α, IL-1β, IL-6) and decreasing the levels of anti-inflammatory factors (IL-10, TGF-β1). As disruption of the intestinal barrier is closely linked to oxidative stress and apoptosis, we have conducted research in both areas for this reason. The results showed that DFZ exposure elevated reactive oxygen species in carp intestines, decreased antioxidant enzyme activity, and suppressed the expression of oxidative stress-related genes. TUNEL results showed that DFZ induced the onset of apoptosis. In addition, the expression levels of apoptosis-related genes and proteins were examined. Western blotting results showed that DFZ could upregulate the protein expression levels of Bax, Cytochrome C and downregulate the protein levels of Bcl-2. qPCR results showed that DFZ could upregulate the transcript levels of Bax, Caspase-3, Caspase-8 and Caspase-9 and downregulate the transcript levels of Bcl-2 transcript levels. This suggests that DFZ can induce apoptosis of mitochondrial pathway in carp intestine. In conclusion, DFZ can induce oxidative stress and apoptosis in carp intestine, leading to the destruction of intestinal physical barrier and the occurrence of inflammation. Our data support the idea that oxidative stress and apoptosis are important triggers of pesticide-induced inflammatory bowel illness.

Protective effect of vitamin C against ethanol induced oxidative stress in Wistar rats

Inflammation is a natural immune response to harmful agents. This study aimed to explore the protective effect of vitamin C against alcohol-induced toxicity on hematological inflammatory markers. Forty healthy adult male Wistar rats were acclimatized and divided into eight groups. Group A served as the control, while Group B received alcohol. Groups C, D, and E were given varying doses of vitamin C, and Groups F, G, and H received alcohol followed by vitamin C treatments. After twenty-one days, blood samples were collected and analyzed for various markers. Rats receiving alcohol only showed increased white blood cell count (WBC), platelet count (PLT), neutrophil to lymphocyte ratio (NLR), and platelet to lymphocyte ratio (PLR), along with decreased antioxidant enzyme activity. However, rats receiving vitamin C alone or in combination with alcohol exhibited reduced inflammatory markers and increased antioxidant activity compared to the alcohol-only group. The study demonstrated that commercial-grade vitamin C at doses of 100 mg/kg, 200 mg/kg, and 300 mg/kg effectively reduced chronic low-grade inflammation. Overall, the findings suggest that vitamin C supplementation may mitigate the inflammatory effects of alcohol consumption.

Regulation of soybean drought response by mepiquat chloride pretreatment.

Soybean is the world's most important cultivated crop, and drought can affect their growth and, eventually, yields. Foliar application of mepiquat chloride (MC) can potentially alleviate the damage caused by drought stress in plants; however, the mechanism of MC regulation of soybean drought response has not been studied. This study investigated the mechanism of soybean drought response regulation by mepiquat chloride in two varieties of soybean, sensitive Heinong 65 (HN65) and drought-tolerant Heinong44 (HN44), under three treatment scenarios, normal, drought stress, and drought stress + MC conditions. MC promoted dry matter accumulation under drought stress, reduced plant height, decreased antioxidant enzyme activity, and significantly decreased malondialdehyde content. The light capture processes, photosystems I and II, were inhibited; however, accumulation and upregulation of several amino acids and flavonoids by MC was observed. Multi-omics joint analysis indicated 2-oxocarboxylic acid metabolism and isoflavone biosynthetic pathways to be the core pathways by which MC regulated soybean drought response. Candidate genes such as LOC100816177, SOMT-2, LOC100784120, LOC100797504, LOC100794610, and LOC100819853 were identified to be crucial for the drought resistance of soybeans. Finally, a model was constructed to systematically describe the regulatory mechanism of MC application in soybean under drought stress. This study fills the research gap of MC in the field of soybean resistance.

Implication of Lupeol in compensating Sorafenib-induced perturbations of redox homeostasis: A preclinical study in mouse model

AimsCancer chemotherapeutic drugs can potentially cause several adverse effects that influence a patient's general well-being. Sorafenib, an approved drug used in clinics against multiple cancers whose overall efficacy suffered a serious setback due to various side effects, leading to its frequent discontinuation. Lupeol has recently been considered an important prospective therapeutic agent due to its low toxicity and enhanced biological efficacy. Hence, our study aimed to evaluate whether Lupeol can perturb the Sorafenib-induced toxicity. Main methodsTo test our hypothesis, we studied DNA interaction, level of cytokines, LFT/RFT, oxidant/antioxidant status, and their influences on genetic, cellular, and histopathological changes using both in vitro and in vivo models. Key findingsThe Sorafenib-treated group showed a marked increase in reactive oxygen and nitrogen species (ROS/RNS), an increase in liver and renal function marker enzymes, serum cytokines (IL-6, TNF-α, IL-1β) macromolecular damages (protein, lipid, and DNA), and a decrease in antioxidant enzymes (SOD, CAT, TrxR, GPx, GST). Moreover, Sorafenib-induced oxidative stress caused marked cytoarchitectural damage in the liver and kidney and increased p53 and BAX expression. Interestingly, combining Lupeol with Sorafenib improves all the examined toxic insults caused by Sorafenib. In conclusion, our findings suggest that Lupeol can be used in combination with Sorafenib to reduce ROS/RNS-induced macromolecule damage, which might result in hepato-renal toxicity. SignificanceThis study presents the possible protective effect of Lupeol against Sorafenib-induced adverse effects by perturbing redox homeostasis imbalance and apoptosis leading to tissue damage. This study is a fascinating finding that warrants further in-depth preclinical and clinical studies.

Hesperidin has a protective effect on paclitaxel-induced testicular toxicity through regulating oxidative stress, apoptosis, inflammation and endoplasmic reticulum stress

Paclitaxel (PTX) is widely used to treat a number of malignancies, although it has toxic side effects. Hesperidin (HES) has a wide range of biological and pharmacological properties, including anti-inflammatory and antioxidant abilities. This research aims to investigate the role of HES in PTX-induced testicular toxicity. For 5 days, 2 mg/kg/bw i.p. of PTX was administered to induce testicular toxicity. Rats were administered oral dosages of 100 and 200 mg/kg/bw HES for 10 days after PTX injection. The mechanisms of inflammation, apoptosis, endoplasmic reticulum (ER) stress, and oxidants were investigated using biochemical, genetic, and histological techniques. As a result of PTX administration, decreased antioxidant enzyme (superoxide dismutase, catalase, and glutathione peroxidase) activities and increased malondialdehyde level were regulated, and the severity of oxidative stress was reduced. NF-κB, IL-1β and TNF-α levels, which are among the increased inflammation parameters caused by PTX, decreased with HES administration. Although AKT2 gene expression decreased in PTX administered rats, it was determined that HES administration up-regulated AKT2 mRNA expression. Anti-apoptotic Bcl-2 decreased with PTX administration, and apoptotic Bax and Caspase-3 increased while HES administration reverted these effects towards control level. As a result of toxicity, the increase in ATF6, PERK, IRE1α, GRP78 levels caused prolonged ER stress, and this activity was diminished with HES and tended to regress. While all data were evaluated, Paclitaxel caused damage by increasing inflammation, apoptosis, ER stress and oxidant levels in testicular tissue, and Hesperidin showed a protective effect by correcting the deterioration in these levels.

Bio-efficacy of aluminum phosphide and cypermethrin against some physiological and biochemical aspects of Chrysomya megacephala maggots

Carrion flies play a significant role in forensic entomotoxicology, where they are employed as alternative samples when traditional samples are unavailable. In situations of poisoned death, these toxins disrupt insect development and affect forensic entomology analyses. So, forensic entomotoxicologists must be aware of this impact. The present study aimed to determine the effects of aluminum phosphide (AlP) and cypermethrin (CP) on the biochemical parameters and antioxidant enzymes of the third instar of Chrysomya megacephala maggots. C. megacephala was reared on normal and poisoned rabbit carcasses with aluminum phosphide and cypermethrin. The third larval instar of C. megacephala was studied using by spectrophotometer for detection of total protein, (TP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), total antioxidant capacity (TAC), superoxide dismutase (SOD), glutathione s-transferase (GST), catalase (CAT) and malondialdehyde (MDA). The results indicated to significantly decrease of TP, TAC, SOD, GST and CAT and increase of AST, ALT and MDA in the maggots reared on the poisoned carcasses with AlP or CP compared with control group. In conclusion, the tested insecticides brought about a decrease antioxidant enzyme activity and increase of MDA could be involved in free radicals in C. megacephala larvae leading to oxidative stress by these insecticidal components.

IAA-decorated CuO nanocarriers significantly improve Chickpea growth by increasing antioxidative activities.

Plant growth regulators tagged on metallic oxide nanoparticles (NPs) may function as nanofertilizers with reduced toxicity of NPs. CuO NPs were synthesized to function as nanocarriers of Indole-3-acetic acid (IAA). Powder X-ray diffraction (XRD) and scanning electron microscopy (SEM) revealed 30.4nm size of NPs and sheet-like structure, respectively, of CuO-IAA NPs. Fourier-transform infrared spectroscopy (FTIR) confirmed CuO-IAA formation. IAA-decorated CuO NPs enhanced the physiological parameters of Chickpea plants, i.e., root length, shoot length, and biomass compared to naked CuO NPs. The variation in physiological response was due to change of phytochemical contents in plants. Phenolic content increased up to 17.98 and 18.13 µgGAE/mg DW at 20 and 40mg/L of CuO-IAA NPs, respectively. However, significant decrease in antioxidant enzymes' activity was recorded compared to control. Presence of CuO-IAA NPs increased the reducing potential of plants at higher concentration of NPs, while decrease in total antioxidant response was observed. This study concludes that IAA conjugation to CuO NPs reduces toxicity of NPs. Furthermore, NPs can be explored as nanocarriers for plant modulators and slow release in future studies.

BrDMC1, a Recombinase Gene, Is Involved in Seed Germination in Brassica rapa under Salt Stress

Recombinases are in part responsible for homologous recombination and genome integrity during DNA repair. DMC1 has a typical RecA domain, and belongs to the recombinase superfamily. The reactive oxygen species (ROS) as a potent DNA damage agent is produced during seed germination under stress conditions. DNA repair should be initiated immediately to allow for subsequent seedling development. In this study, we attempted to characterize the underlying mechanism of BrDMC1 responsiveness to salinity stress using the RNA interference approach in Brassica rapa (B. rapa). Bioinformatics and expression pattern analysis revealed that BrDMC1 only retained BrDMC1.A01 after the whole genome triplication (WGT) event and was primarily transcribed in flowers and seeds. BrDMC1 had high activity in the promoter region during germination, according to histochemical GUS staining. The data showed that salt treatment reduced the germination rate, weakened seed vigor and decreased antioxidant enzyme activity, but increased oxidative damage in BrDMC1-RNAi seeds. Furthermore, the expression of stress-responsive genes and damage repair genes was significantly different in transgenic lines exposed to salt stress. Therefore, BrDMC1 may respond to salt stress by controlling seed germination and the expression of stress-related and damage repair genes in B. rapa.

Oxidative stress and neuroimmune proteins in a mouse model of autism.

Oxidative stress including decreased antioxidant enzyme activities, elevated lipid peroxidation, and accumulation of advanced glycation end products in the blood from children with autism spectrum disorders (ASD) has been reported. The mechanisms affecting the development of ASD remain unclear; however, toxic environmental exposures leading to oxidative stress have been proposed to play a significant role. The BTBRT+Itpr3tf/J (BTBR) strain provides a model to investigate the markers of oxidation in a mouse strain exhibiting ASD-like behavioral phenotypes. In the present study, we investigated the level of oxidative stress and its effects on immune cell populations, specifically oxidative stress affecting surface thiols (R-SH), intracellular glutathione (iGSH), and expression of brain biomarkers that may contribute to the development of the ASD-like phenotypes that have been observed and reported in BTBR mice. Lower levels of cell surface R-SH were detected on multiple immune cell subpopulations from blood, spleens, and lymph nodes and for sera R-SH levels of BTBR mice compared to C57BL/6J (B6) mice. The iGSH levels of immune cell populations were also lower in the BTBR mice. Elevated protein expression of GATA3, TGM2, AhR, EPHX2, TSLP, PTEN, IRE1α, GDF15, and metallothionein in BTBR mice is supportive of an increased level of oxidative stress in BTBR mice and may underpin the pro-inflammatory immune state that has been reported in the BTBR strain. Results of a decreased antioxidant system suggest an important oxidative stress role in the development of the BTBR ASD-like phenotype.

RETRACTED: Exercise ameliorates hippocampal damage induced by Wi-Fi radiation; a biochemical, histological, and immunohistochemical study

IntroductionNowadays, using electromagnetic devices (EMD) has been increased. However, the control of EMD hazards was poorly evaluated, especially those affected the hippocampus. Regular physical exercises are safe, easily, inexpensive, and acceptable for long-term use. It is reported that exercise protects against many health problems. Aimis to investigate the hypothesis of the possible prophylactic effect of exercise on the hippocampal damage induced by electromagnetic waves of Wi-Fi. Material and methodsAdult male albino rats were divided into four groups: group I (control), group II (exercise), group III (Wi-Fi), and group IV (exercise -Wi-Fi). Hippocampi were subjected to biochemical, histological, and immunohistochemical techniques. ResultsIn group III, a significant increase in the oxidative enzymes as well as decrease in antioxidant enzymes were detected in rat hippocampus. Additionally, the hippocampus showed degenerated pyramidal and granular neurons. An evident decrease in both PCNA and ZO-1 immunoreactivity was also noticed. In group IV, physical exercise alleviates the effect of Wi-Fi on previously mentioned parameters. ConclusionRegular physical exercise performance significantly minimizes the hippocampal damage and protects against the hazarders of chronic Wi-Fi radiation exposure.