Superoxide Dismutase Gene Research Articles

Genome-wide identification of the rubber tree superoxide dismutase (SOD) gene family and analysis of its expression under abiotic stress.

BackgroundThe rubber tree (Hevea brasiliensis) is the only species capable of producing high-quality natural rubber for commercial use, and is often subjected to various abiotic stresses in non-traditional rubber plantation areas. Superoxide dismutase (SOD) is a vital metalloenzyme translated by a SOD gene family member and acts as a first-line of protection in plant cells by catalysing the disproportionation of reactive oxygen species (ROS) to produce H2O2 and O2. However, the SOD gene family is not reported in rubber trees.MethodsHere, we used hidden markov model (HMM) and BLASTP methods to identify SOD genes in the H. brasiliensis genome. Phylogenetic tree, conserved motifs, gene structures, cis elements, and gene ontology annotation (GO) analyses were performed using MEGA 6.0, MEME, TBtools, PlantCARE, and eggNOG database, respectively. HbSOD gene expression profiles were analysed using quantitative reverse transcription polymerase chain reaction (qRT-PCR).ResultsWe identified nine HbSOD genes in the rubber tree genome, including five HbCSDs, two HbFSDs, and two HbMSDs. Phylogenetic relationship analysis classified the SOD proteins from the rubber tree and other related species into three subfamilies. The results of gene structure and conserved motif analysis illustrated that most HbSOD genes have similar exon-intron numbers and conserved motifs in the same evolutionary branch. Five hormone-related, four stress-related, and light-responsive elements were detected in the HbSODs’ promoters. HbSODs were expressed in different tissues, gradually increased with leaf development, and were abundantly expressed in mature leaves. HbCSD2 and HbCSD4 was significantly upregulated under low and high temperatures, and salt stress, except for HbCSD2, by heat. Furthermore, most HbSOD genes were significantly upregulated by drought, except HbMSD2. These findings imply that these genes may play vital roles in rubber tree stress resistance. Our results provide a basis for further studies on the functions of HbSOD genes in rubber trees and stress response mechanisms.

Three Heat Shock Protein Genes and Antioxidant Enzymes Protect Pardosa pseudoannulata (Araneae: Lycosidae) from High Temperature Stress.

Pardosa pseudoannulata (P. pseudoannulata) is an essential natural predatory enemy in rice ecosystems. The fluctuating climate may cause them to experience heat stress, whereas heat shock proteins (HSPs) and antioxidant enzymes help resist heat damage. Herein, we cloned and characterized the full-length genes PpHSP27, PpHSP60, and PpHSC70 from P. pseudoannulata. Changes in gene expression levels and superoxide dismutase (SOD), catalase (CAT), and glutathione transferase (GST) activities in adult male and female P. pseudoannulata were measured at different stress exposure times and temperatures. We found that the abovementioned HSP genes belong to the sHSP, HSP60, and HSP70 families. The expression of the three HSP genes and the activities of SOD, CAT, and GST were significantly upregulated with the increasing stress temperature and time. The knockdown of the three HSP genes via RNA interference significantly decreased the survival rate of male and female P. pseudoannulata during high temperature stress. Thus, PpHSP27, PpHSP60, and PpHSC70 play an important role in the heat tolerance of P. pseudoannulata, and SOD, CAT, and GST enable recovery heat stress-induced oxidative damage. Their changes and regulation during high temperature stress can improve spiders' adaptability in the field and enhance the biological control of environmental pests.

Evaluation of metabolic stress status in common carp (Cyprinus carpio) exposed to the fungicide folpet

Among pesticides, fungicides are the most extensively used ones in agriculture and their effects on fish health and indirectly human health are needed to evaluate. Folpet has been used for over 50 years as a fungicide across the world. The mechanism of action of folpet on non-target aquatic organisms is so poorly understood and there is no available information about potential acute toxicity of folpet and its mechanism of action in non-target aquatic organisms. With this motivation, two successive experiments were set up: first, 96 h-LC50 value of folpet for common carp (Cyprinus carpio) was determined; and second, effects of different sublethal concentrations (0, 0.025, 0.50, 0.1 and 0.15 mg/L) of folpet on hematological serum biochemical blood parameters, DNA damages, expression levels of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione S-transferase (GST), and cortisol receptor (HSP70) genes were evaluated in this study. It was calculated that 0.199 mg/L of folpet was the 96 h-LC50 value. After the folpet exposure for 14 days, significant decreases in red blood cells, hemoglobin, hematocrit, serum total protein, and GST gene expression levels were observed while serum glucose, liver enzymes activities, and expression levels of CAT, SOD, GPx, HSP70 genes increased. Also, folpet induced a significant genotoxic effect on the blood cells regarding to DNA damages. Consequently, the results have shown the toxic effects of folpet even at the lowest concentration on common carp.

Antioxidant and anti-apoptotic effects of selenium nanoparticles and Lactobacillus casei on mice testis after X-ray.

Radiation can lead to various damages in the process of spermatogenesis that lead to a decrease in the number of sperm, an increase in spermatogenesis disorders, and defective sperm function. Radioprotectors are considered a good approach to reducing the damage caused by radiation. The goal of this work was to study how X-ray radiation affects testicular tissue and the process of spermatogenesis, as well as the radioprotective effects of selenium nanoparticles (SeNPs) and Lactobacillus casei (L. casei) as probiotic compounds, given alone or together. This study included 64 adult Syrian male mice weighing approximately 20 ± 5 g and aged 10 ± 1 weeks. Animals were randomly divided into eight groups: control group, SeNPs, probiotic, SeNPs and probiotic, X-ray radiation, SeNPs (X-ray), probiotic (X-ray), and SeNPs and probiotic (X-ray). Histology parameters and levels of oxidative stress biomarkers such as catalase, malondialdehyde, superoxide dismutase, and glutathione peroxidase were examined. In addition, the level of apoptosis was measured in testicular cells that had been treated with SeNPs and L. casei as a probiotic. The results showed that the administration of SeNPs or probiotic diminished the effects of X-ray radiation. These compounds induced a significant decreased in malondialdehyde, caspase 3, and caspase 9 gene levels and a remarkable increased in catalase, superoxide dismutase, and Catsper gene expression. SeNPs and probiotic exhibited a potent antioxidant effect and elevated the mean number of spermatogonia cells, sperm cell count, spermatogenesis percentage, and sperm motility percentage. The prescribed compound exhibited an ideal radioprotective effect with the ability to reduce the side effects of ionizing radiation and to protect normal tissues. SeNPs and probiotic inhibit testicular injury and improve the antioxidant state in male mice.

Mutation-specific metabolic profiles in presymptomatic amyotrophic lateral sclerosis.

Growing evidence shows that ALS patients feature a disturbed energy metabolism. However, these features have rarely been investigated in the presymptomatic stage. A total of 60 presymptomatic ALS mutation carriers and 70 age- and gender-matched controls (non-mutation carriers from the same families) were recruited. All subjects underwent assessments of their metabolic profiles under fasting conditions at enrollment, including body mass index (BMI), blood pressure and serum levels of blood glucose, total cholesterol, triglycerides, high-density lipoprotein (HDL) and low-density lipoprotein. All mutations combined, no differences between presymptomatic ALS gene carriers and controls were found. From a cardiovascular point of view, presymptomatic chromosome 9 open reading frame 72 (C9ORF72) gene carriers showed lower cardiovascular risk profiles compared to healthy controls, including lower BMI (median 22.9, interquartile range [IQR] 20.6-26.1 kg/m2 vs. 24.9, IQR 22.7-30.5 kg/m2 ; p=0.007), lower systolic blood pressure (120, IQR 110-130 mmHg vs. 128, IQR 120-140 mmHg; p=0.02), lower fasting serum glucose (89.0, IQR 85.0-97.0 mg/dl vs. 96.0, IQR 89.3-102.0 mg/dl; p=0.005) and higher HDL (1.6, IQR 1.3-1.8 mmol/l vs. 1.2, IQR 1.0-1.4 mmol/l; p=0.04). However, presymptomatic superoxide dismutase 1 (SOD1) gene mutation carriers showed higher cardiovascular risk profiles compared to healthy controls, including higher BMI (28.0,IQR 26.1-31.5 kg/m2 vs. 24.9, IQR 22.7-30.5 kg/m2 ; p=0.02), higher fasting serum glucose (100.0, IQR 94.0-117.0 mg/dl vs. 96.0, IQR 89.3-102.0 mg/dl; p=0.04) and lower HDL (1.2, IQR 1.0-1.4 mmol/l vs. 1.4, IQR 1.2-1.7 mmol/l; p=0.01). These features were most prominent in patients carrying SOD1 gene mutations associated with slow disease progression. This study identified distinct metabolic profiles in presymptomatic ALS gene carriers, which might be associated with disease progression in the symptomatic phase.

Investigation of sod2 gene polymorphism in the patients associated with type-2 diabetes mellitus patients

Introduction: Type-2 Diabetes mellitus (type-2DM) is a multifactorial metabolic disorder, characterized by hyperglycemia. Oxidative stress plays a crucial role in the progression of diabetes and its complications. The polymorphism in the SOD2 gene (superoxide dismutase) results in minimal production of SOD enzymes, which may affect the scavenging of free radicals. Aim: to see the level of SOD enzyme in type-2DM patients associated with SOD2 gene polymorphism. Material& Methods: It is a comparative study conducted in the department of anatomy in collaboration with the Department of General Medicine, RKDF medical college Hospital& research center, Bhopal. 5 ml of venous blood from type-2 DM patients (n=30) and control subject (n=30) was collected, followed by estimation of blood glucose (HbA1c, FBS& PPBS) and the genetic test was done to detect the SOD2 gene polymorphism. Results: Blood glucose levels (HbA1c, FBS &PPBS) were high and SOD levels were low in type-2 DM patients when compared with control subjects (p<0.05). When a comparison was done among three genotypes, the levels of SOD enzyme were high in the CC genotype followed by CT and TT genotypes.

Screening of Natural Compounds Against SOD1 as a Therapeutic Target for Amyotrophic Lateral Sclerosis

Background: Amyotrophic lateral sclerosis (ALS) is an uncommon and progressive neurological illness that predominantly includes the neurons liable for voluntary muscular activities. Starting from weakness or stiffness in muscles, this gradually exploits the strength and ability to speak, eat, move, and even breathe. Its exact mechanism is still not clear, but mutations in the SOD1 gene have been reported to cause ALS, and some studies also found involvement of SOD1 overexpression in the pathogenesis of ALS. As of now, there is no remedy available for its cure. Objective: The objective of this study is to identify the potential inhibitors for wild type 1HL5, l113T mutant, and A4V mutant of SOD1 (Superoxide Dismutase 1) protein. Methods: In this study, in silico approaches like virtual screening, molecular docking, pharmacokinetic parameters study, and molecular dynamics simulation were used to identify the best potential inhibitors against wild type and mutant SOD1 protein. Results: On the basis of binding affinity and binding energy, the top three compounds ZINC000095486263, ZINC000095485989, and ZINC000028462577 were observed as the best compounds. In the case of 1HL5, ZINC000095486263 had the highest binding affinity with docking score - 10.62 Kcal/mol, 1UXM with ZINC000095485989 had the highest docking score -12.03 Kcal/mol, and 4A7V with ZINC000028462577 was found -11.72 Kcal/mol. Further, Molecular Dynamic Simulations (MDS) results showed that the ZINC000095486263, ZINC000095485989, and ZINC000095485956 compounds were formed a stable complex with 1HL5, 1UXM, and 4A7V respectively. Conclusions: After analyzing the results, we hereby conclude that natural compounds such as ZINC000095486263, ZINC000095485989, and ZINC000095485956 could be used as a potential inhibitor of 1HL5, 1UXM, and 4A7V respectively for ALS treatment and could be used as a drug. Further, In vivo/vitro study of these compounds could be a future direction in the field of drug discovery.

Integrative Analysis of Motor Neuron and Microglial Transcriptomes from SOD1G93A Mice Models Uncover Potential Drug Treatments for ALS.

Amyotrophic lateral sclerosis (ALS) is a fatal disease of motor neurons that mainly affects the motor cortex, brainstem, and spinal cord. Under disease conditions, microglia could possess two distinct profiles, M1 (toxic) and M2 (protective), with the M2 profile observed at disease onset. SOD1 (superoxide dismutase 1) gene mutations account for up to 20% of familial ALS cases. Comparative gene expression differences in M2-protective (early) stage SOD1G93A microglia and age-matched SOD1G93A motor neurons are poorly understood. We evaluated the differential gene expression profiles in SOD1G93A microglia and SOD1G93A motor neurons utilizing publicly available transcriptomics data and bioinformatics analyses, constructed biomolecular networks around them, and identified gene clusters as potential drug targets. Following a drug repositioning strategy, 5 small compounds (belinostat, auranofin, BRD-K78930611, AZD-8055, and COT-10b) were repositioned as potential ALS therapeutic candidates that mimic the protective state of microglia and reverse the toxic state of motor neurons. We anticipate that this study will provide new insights into the ALS pathophysiology linking the M2 state of microglia and drug repositioning.

Influences of ferulic acid on intestinal digestive and antioxidant enzymes, immune, antioxidant gene and tight junction protein expression and microbiota in hybrid grouper (Epinephelus fuscoguttatus♀× Epinephelus polyphekadion♂)

The current study was performed to assess the effects of dietary administration of ferulic acid (FA) on digestive enzyme activities, antioxidant capacity, morphology, immunity, and microbiota in the gut of hybrid grouper (Epinephelus fuscoguttatus♀ × Epinephelus polyphekadion♂). A total of 630 fish (9.51 ± 0.01 g) were allocated randomly to seven dietary treatments, each with three replicates. Experiment diets supplemented with FA at the levels of 0, 40, 80, 160, 320, 640, and 1280 mg kg−1 (FA0 (control), FA40, FA80, FA160, FA320, FA640, and FA1280), were fed to fish for 70 days. The results showed that dietary 80–160 mg kg−1 FA intake considerably augmented the enzymes activities of digestion (lipase, trypsin, amylase, and pepsin) and antioxidation (superoxide dismutase, glutathione peroxidase, and catalase) and the values of immune parameters (Immunoglobulin, C3 and lysozyme), as well as reduced malondialdehyde content, with respect to the control group (P < 0.05). Furthermore, a significant increase in the intestinal fold height, fold width, and muscular thickness was detected in fish fed the diets containing 80–160 mg kg−1 FA (P < 0.05). For gut genes expression, dietary supplementation of 80–160 mg kg−1 FA significantly upregulated the transcriptional levels of the immune-related genes (interleukin 1β, interleukin 8, tumor necrosis factor-alpha, interleukin 10, and transforming growth factor-beta 1), the antioxidation-associated genes (superoxide dismutase, copper/zinc superoxide dismutase, and nuclear factor erythroid 2-related factor 2-like 2), and tight junction proteins genes (zonula occludens 1, Occludin, and Claudin-3), whereas downregulated kelch like ECH associated protein 1 (P < 0.05). Regarding the intestinal microbiota, the FA-supplemented diets with 80 and 1280 mg kg−1 significantly increased the alpha diversity indexes (Simpson and Shannon) and the relative abundances of Firmicutes and Bacteroidetes, as well as lowered the relative abundance of Proteobacteria (P < 0.05). Additionally, the ratio of Firmicutes to Bacteroidetes was remarkably reduced, following the diet supplemented with 80 mg kg−1 FA, which also exhibited the decreased relative abundance of Acinetobacter and the increased relative abundances of Lactobacillus and Bifidobacterium (P < 0.05). Taken together, these results signified that the appropriate FA inclusion in diets could serve as a nutritional strategy to improve the intestinal health of hybrid grouper.

Effect of long-term manganese exposure on oxidative stress, liver damage and apoptosis in grouper Epinephelus moara ♀ × Epinephelus lanceolatus ♂

Manganese is an indispensable trace element, however, it may be present at high concentrations in water and sediments of aquatic ecosystems due to natural and anthropogenic activities, and can interfere with physiological and biochemical mechanisms in fish. This study was conducted to determine the toxic effects associated with exposure to Mn2+ (0, 0.5, 1, 2, and 4 mg/L) for 30 d, regarding liver damage and apoptosis in Yunlong grouper (Epinephelus moara♀×E. lanceolatus♂). Expression of superoxide dismutase (sod) and catalase (cat) genes in the liver was significantly increased on days 10 and 20 following Mn2+ exposure (4 mg/L), but was reduced on day 30. Similarly, expression of glutathione peroxidase (gpx) and glutathione reductase (gr) genes was elevated after 10 d of exposure to 2 and 4 mg/L Mn2+, but decreased after 20 and 30 d. After 30 d of exposure to high concentrations (2 and 4 mg/L) of Mn2+, liver tissue showed hepatic sinusoidal gap congestion, dilatation, cell vacuolation, and necrosis. In addition, the activities of alanine aminotransferase (ALT) and aspartate transaminase (AST) as well as 8-hydroxydeoxyguanosine (8-OHdG) levels were significantly increased after Mn2+ exposure. Moreover, Mn2+ exposure altered the expression pattern of some pivotal genes associated to apoptosis (p53, bax, bcl-2, apaf-1, caspase-9, and caspase-3), which suggested that Mn2+ exposure induces apoptosis through the mitochondrial pathway. The above results showed that excessive Mn2+ induced apoptosis and liver damage in grouper through elicitation of oxidative stress. These insights help elucidate the mechanism by which Mn2+ induces toxicity in marine fish, and provide a new perspective regarding the detrimental effects of heavy metals in fish.

Insights to the superoxide dismutase genes and its roles in Hevea brasiliensis under abiotic stress.

The online version contains supplementary material available at 10.1007/s13205-022-03328-7.

Melatonin alleviates chilling injury and maintains postharvest quality by enhancing antioxidant capacity and inhibiting cell wall degradation in cold-stored eggplant fruit

Melatonin improves the chilling tolerance and quality of postharvest fruit. In this study, we investigated the effect of melatonin on postharvest quality in cold-stored eggplant fruit for 30 d at 5 °C. Melatonin at 100 μmol L−1 was notably effective in decreasing chilling injury (CI) incidence, CI index, weight loss, and in delaying the decrease of lightness, thereby maintaining better postharvest quality of the fruit. Exogenous melatonin inhibited increases in hydrogen peroxide (H2O2), malondialdehyde (MDA), and relative electro-conductivity in the pericarp and pulp, while maintaining higher levels of superoxide dismutase (SOD), catalase (CAT), total polyamines, anthocyanins, and melatonin, as well as the expressions of SOD, CAT1/2, and other genes involved in polyamine biosynthesis (ADC, ODC), melatonin biosynthesis (TDC1, T5H, SNAT1, ASMT, COMT), anthocyanin biosynthesis (PAL, CHS1, CHI, F3H, F3′H, DFR, ANS, 3GT), and cold regulation (COR1, CBF, ZAT2/6/12), thereby conferring the higher chilling tolerance. Melatonin delayed fruit softening and senescence by inhibiting the activities and gene expressions of cell wall degradation enzymes (PME, PG, Cel) and expressions of senescence-associated genes (IAA17, SAG12, SEN4). Overall, these results indicate that melatonin alleviates chilling injury and maintains postharvest quality by enhancing antioxidant capacity and inhibiting cell wall degradation in cold-stored eggplant fruit, which provides a theoretical foundation for extending fruit shelf-life of eggplant during cold storage.

Testicular Expression of Antioxidant Enzymes and Changes in Response to a Slow-Release Deslorelin Implant (Suprelorin® 4.7 mg) in the Dog.

Simple SummaryWe investigated the expression of the testicular antioxidant enzyme system, i.e., superoxide dismutase (SOD1 and 2), catalase (CAT), glutathione peroxidase (GPx1), and glutathione disulfide reductase (GSR), in healthy adult and prepubertal dogs and after slow-release GnRH superagonist deslorelin (Suprelorin® 4.7 mg subcutaneous implant, Virbac, France) treatment in adult dogs. qPCR and immunohistochemistry were used to detect gene expression and protein expression and localization, respectively. These antioxidant enzymes were variably expressed within cellular compartments in the seminiferous epithelium and the interstitium. SOD1, CAT, and GSR protein expression were also dependent on the stage of the seminiferous epithelium cycle in normal adult dogs. Deslorelin treatment and prepubertal status affected the expression and localization of the investigated antioxidant enzymes. Our results confirmed the presence of a functional antioxidant enzyme system in the canine testis, which was also observed during deslorelin-induced spermatogenic and steroidogenic arrest, as well as in prepubertal dogs. These results improve our current understanding of the local antioxidant protective mechanisms within the testis in the dog. Spermatogenesis takes place in a hypoxic environment, and antioxidant enzymes protect germ and somatic cells from free radical-mediated damage. Expression of the antioxidant enzyme system in the canine testis has not yet been investigated. We hypothesized that the slow-release GnRH superagonist deslorelin 4.7 mg implant, which induces temporary reversible suppression of endocrine and germinative testicular function, would affect the testicular expression of antioxidant enzymes compared to untreated adult and prepubertal dogs. The goal of this study was to investigate and compare gene (by qPCR, in whole-tissue homogenates) and protein expression (by immunohistochemistry) of superoxide dismutase (SOD1, SOD2), catalase (CAT), glutathione peroxidase (GPx1), and glutathione disulfide reductase (GSR) in the testes of untreated adult (CON, n = 7), prepubertal (PRE, n = 8), and deslorelin-treated (DES, n = 5, 16 weeks after implantation) dogs. We found that in DES dogs, the gene expression of SOD1 was significantly (p < 0.05) lower and GPx1 was higher than in CON, and SOD2 was higher than in PRE. Expression of all, except for the SOD2 mRNA, differed between the CON and PRE dogs. Immunohistochemistry showed distinct cell-specific localization and expression patterns for the antioxidant enzymes in each experimental group. Additionally, in the CON animals, cell-specific SOD1, CAT, and GSR expression was dependent on the stage of the seminiferous epithelium cycle. These findings confirm that members of the antioxidant enzyme system are present in normal adult and prepubertal testis as well as in the deslorelin-treated downregulated adult canine testis, and that this local antioxidant system protects developing germ cells and somatic cells from oxidative damage. Different expression patterns of antioxidant enzymes in various germ cell populations and stages of the seminiferous epithelium cycle may indicate differences in their susceptibility to oxidative stress depending on their developmental and maturation stage. The continued presence of the antioxidant enzymes in the testis of DES dogs offers protection to spermatogonia as well as Sertoli and Leydig cells from oxidative stress during temporary infertility, potentially contributing to ensure the reversibility of suppression and the return of normal spermatogenesis and steroidogenesis after the end of deslorelin treatment.

An R2R3-MYB transcription factor VyMYB24, isolated from wild grape Vitis yanshanesis J. X. Chen., regulates the plant development and confers the tolerance to drought

In grapevines, the MYB transcription factors play an important regulatory role in the phenylpropanoid pathway including proanthocyanidin, anthocyanin, and flavonoid biosynthesis. However, the role of MYB in abiotic stresses is not clear. In this study, an R2R3-MYB transcription factor, VyMYB24, was isolated from a high drought-tolerant Chinese wild Vitis species V. yanshanesis. Our findings demonstrated that it was involved in plant development and drought tolerance. VyMYB24 is a nuclear protein and is significantly induced by drought stress. When over-expressed in tobacco, VyMYB24 caused plant dwarfing including plant height, leaf area, flower size, and seed weight. The GA1+3 content in transgenic plants was reduced significantly, and spraying exogenous gibberellin could recover the dwarf phenotype of VyMYB24 transgenic plants, suggesting that VyMYB24 might inhibit plant development by the regulation of gibberellin (GA) metabolism. Under drought stress, the VyMYB24 transgenic plants improved their tolerance to drought with a lower wilting rate, lower relative electrical conductivity, and stronger roots. Compared to wild-type tobacco plants, VyMYB24 transgenic plants accumulated less reactive oxygen, accompanied by increased antioxidant enzyme activity and upregulated gene expression levels of superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT) genes. In addition, transgenic plants accumulated more proline, and their related synthetic genes NtP5CR and NtP5CS genes were significantly upregulated when exposed to drought. Besides, abiotic stress-responsive genes, NtDREB, NtERD10C, NtERD10D, and NtLEA5, were upregulated significantly in VyMYB24 transgenic plants. These results indicate that VyMYB24 plays a positive regulatory role in response to drought stress and also regulates plant development, which provides new evidence to further explore the molecular mechanism of drought stress of the MYB gene family.

Evaluation of the Effect of the Fibroblast Growth Factor Type 2 (FGF-2) Administration on Placental Gene Expression in a Murine Model of Preeclampsia Induced by L-NAME.

The abnormal implantation of the trophoblast during the first trimester of pregnancy precedes the appearance of the clinical manifestations of preeclampsia (PE), which is a hypertensive disorder of pregnancy. In a previous study, which was carried out in a murine model of PE that was induced by NG-nitro-L-arginine methyl ester (L-NAME), we observed that the intravenous administration of fibroblast growth factor 2 (FGF2) had a hypotensive effect, improved the placental weight gain and attenuated the fetal growth restriction, and the morphological findings that were induced by L-NAME in the evaluated tissues were less severe. In this study, we aimed to determine the effect of FGF2 administration on the placental gene expression of the vascular endothelial growth factor (VEGFA), VEGF receptor 2 (VEGFR2), placental growth factor, endoglin (ENG), superoxide dismutase 1 (SOD1), catalase (CAT), thioredoxin (TXN), tumor protein P53 (P53), BCL2 apoptosis regulator, Fas cell surface death receptor (FAS), and caspase 3, in a Sprague Dawley rat PE model, which was induced by L-NAME. The gene expression was determined by a real-time polymerase chain reaction using SYBR green. Taking the vehicle or the L-NAME group as a reference, there was an under expression of placental VEGFA, VEGFR2, ENG, P53, FAS, SOD1, CAT, and TXN genes in the group of L-NAME + FGF2 (p < 0.05). The administration of FGF2 in the murine PE-like model that was induced by L-NAME reduced the effects that were generated by proteinuria and the increased BP, as well as the response of the expression of genes that participate in angiogenesis, apoptosis, and OS. These results have generated valuable information regarding the identification of molecular targets for PE and provide new insights for understanding PE pathogenesis.

An accidental discovery of mannan-oligosaccharide's protection effect against air exposure and its potential mechanism in hybrid grouper (Epinephelus lanceolatus ♂ × Epinephelus fuscoguttatus ♀).

The original objective was to explore the potential benefiting effects of three prebiotics in hybrid grouper (Epinephelus lanceolatus♂ × Epinephelus fuscoguttatus♀). Therefore, three experimental diets (basal diet + 1% fructooligosaccharide, Diet F; basal diet + 1% inulin, Diet I; basal diet + 0.3% mannan-oligosaccharide, Diet M) and one basal diet (Diet C) were prepared and a feeding trial was conducted. However, at the end of the fourth week into the feeding experiment, a water-leaking accident occurred and fishes of all groups went through an unexpected air exposure event. Surprisingly, different prebiotic-supplemented groups showed significantly different air exposure tolerance: the mortality of M group was significantly lower (P ≤ 0.05) than all the other groups. Examination of antioxidant, non-specific immunity, and stress parameters revealed that comparing to control group, M group showed significantly increased catalase (CAT), acid phosphatase (ACP), and alkaline phosphatase (AKP) activities, decreased superoxide dismutase (SOD) activity, and similar cortisol level (P ≤ 0.05). Real-time PCR experiment revealed that M group significantly increased the expression of CAT, glutathione peroxidase (GPx), and manganese superoxide dismutase (MnSOD) genes in head kidney (P ≤ 0.05). Overall, M exhibited the best anti-air exposure/antioxidative stress effects among the three prebiotics and could be considered a promising feed additive to relieve air exposure/oxidative stress in hybrid grouper culture.

Perfluorobutanoic Acid (PFBA) Induces a Non-Enzymatic Oxidative Stress Response in Soybean (Glycine max L. Merr.).

Short-chain perfluoroalkyl substances (PFAS) are generally considered to be of less environmental concern than long-chain analogues due to their comparatively shorter half-lives in biological systems. Perfluorobutanoic acid (PFBA) is a short-chain PFAS with the most root–shoot transfer factor of all PFAS. We investigated the impact of extended exposure of soybean plants to irrigation water containing environmentally relevant (100 pg–100 ng/L) to high (100 µg–1 mg/L) concentrations of PFBA using phenotypical observation, biochemical characterization, and transcriptomic analysis. The results showed a non-monotonous developmental response from the plants, with maximum stimulation and inhibition at 100 ng/L and 1 mg/L, respectively. Higher reactive oxygen species and low levels of superoxide dismutase (SOD) and catalase (CAT) activity were observed in all treatment groups. However transcriptomic analysis did not demonstrate differential expression of SOD and CAT coding genes, whereas non-enzymatic response genes and pathways were enriched in both groups (100 ng/L and 1 mg/L) with glycine betaine dehydrogenase showing the highest expression. About 18% of similarly downregulated genes in both groups are involved in the ethylene signaling pathway. The circadian rhythm pathway was the only differentially regulated pathway between both groups. We conclude that, similar to long chain PFAS, PFBA induced stress in soybean plants and that the observed hormetic stimulation at 100 ng/L represents an overcompensation response, via the circadian rhythm pathway, to the induced stress.

Physiological and Molecular Responses of Vitis vinifera cv. Tempranillo Affected by Esca Disease.

Esca is a multi-fungal disease affecting grapevines. The objective of the study was to evaluate the physiological and molecular response of the grapevine cv. Tempranillo to esca disease, carried out in a vineyard under Mediterranean climatic conditions in western Spain. The photosynthetic pigments in the leaves decreased, with a strong decrease in the photosynthetic efficiency. The proline content increased significantly in the early stages of affected leaves, being possibly involved in the maintenance of lipid peroxidation levels in leaves, which do not increase. The phenol, flavonoid, and phenylpropanoid content decreased in esca-affected leaves, as does the total antioxidant capacity (FRAP), while the polyphenol oxidase (PPO) activity suffers a strong increase with the development of the disease. In affected grapes, the lipid peroxidation and the total phenol content decrease, but not the anthocyanin content. The ascorbate pool decreases with the disease and with time. On the other hand, pool GSH + GSSG is lower in affected leaves, but increases with time. These alterations show a clear change in the redox homeostasis. The expression of genes phenylalanine ammonia lyase (PAL), polyphenol oxidase (PPO), superoxide dismutase (SOD), and chalcone synthase (ChaS1 and ChaS3) become considerably higher in response to esca, being even higher when the infection time increases. The alteration of AsA and GSH levels, phenolic compounds, PPO activity, proline content, and FRAP, together with the increase of the PAL, PPO, SOD, ChaS1, and ChaS3 gene expression, are clearly implicated in the esca response in plants. The expression of these genes, similar to the PPO activity, can be used as markers of state in the development of the disease.

Copper Chaperone for Superoxide Dismutase FoCCS1 in Frankliniella occidentalis May Be Associated with Feeding Adaptation after Host Shifting.

Simple SummaryWestern flower thrips (Frankliniella occidentalis) have a wide range of hosts. Therefore, they can colonize new host plants with each seasonal change. This study examined whether the superoxide dismutase (SOD) gene regulates the feeding adaptation of F. occidentalis after host shifting. The coding sequences for CCS1 and MnSOD2 in F. occidentalis were cloned and the corresponding amino acid sequence was predicted, and the mRNA expression levels of these two genes at different developmental stages were determined. Further, the mRNA expression levels of FoCCS1 and FoMnSOD2 in second-instar larvae and adult females transferred to kidney bean and broad bean plants for rearing were analyzed. Decreasing the mRNA levels of FoCCS1 and SOD activity by RNA interference significantly reduced the survival rate and fecundity of adult F. occidentalis females. These findings provide a reference for analyzing the adaptive mechanism of F. occidentalis after host shifting.Western flower thrips (Frankliniella occidentalis) pose a serious threat to the global vegetable and flower crop production. The regulatory mechanism for superoxide dismutase (SOD) in the feeding adaptation of F. occidentalis after host shifting remains unclear. In this study, the copper chaperone for SOD (CCS) and manganese SOD (MnSOD) genes in F. occidentalis were cloned, and their expression levels at different developmental stages was determined. The mRNA expression of FoCCS1 and FoMnSOD2 in F. occidentalis second-instar larvae and adult females of F1, F2, and F3 generations was analyzed after shifting the thrips to kidney bean and broad bean plants, respectively. The F2 and F3 second-instar larvae and F2 adult females showed significantly upregulated FoCCS1 mRNA expression after shifting to kidney bean plants. The F1 second-instar larvae and F2 adult females showed significantly upregulated FoCCS1 mRNA expression after shifting to broad bean plants. The RNA interference significantly downregulated the FoCCS1 mRNA expression levels and adult females showed significantly inhibited SOD activity after shifting to kidney bean and broad bean plants. F. occidentalis adult females subjected to RNA interference and released on kidney bean and broad bean leaves for rearing, respectively, significantly reduced the survival rate and fecundity. These findings suggest that FoCCS1 plays an active role in regulating the feeding adaptation ability of F. occidentalis after host shifting.

Co-deposition of SOD1, TDP-43 and p62 proteinopathies in ALS: evidence for multifaceted pathways underlying neurodegeneration

Multiple neurotoxic proteinopathies co-exist within vulnerable neuronal populations in all major neurodegenerative diseases. Interactions between these pathologies may modulate disease progression, suggesting they may constitute targets for disease-modifying treatments aiming to slow or halt neurodegeneration. Pairwise interactions between superoxide dismutase 1 (SOD1), TAR DNA-binding protein 43 (TDP-43) and ubiquitin-binding protein 62/sequestosome 1 (p62) proteinopathies have been reported in multiple transgenic cellular and animal models of amyotrophic lateral sclerosis (ALS), however corresponding examination of these relationships in patient tissues is lacking. Further, the coalescence of all three proteinopathies has not been studied in vitro or in vivo to date. These data are essential to guide therapeutic development and enhance the translation of relevant therapies into the clinic. Our group recently profiled SOD1 proteinopathy in post-mortem spinal cord tissues from familial and sporadic ALS cases, demonstrating an abundance of structurally-disordered (dis)SOD1 conformers which become mislocalized within these vulnerable neurons compared with those of aged controls. To explore any relationships between this, and other, ALS-linked proteinopathies, we profiled TDP-43 and p62 within spinal cord motor neurons of the same post-mortem tissue cohort using multiplexed immunofluorescence and immunohistochemistry. We identified distinct patterns of SOD1, TDP43 and p62 co-deposition and subcellular mislocalization between motor neurons of familial and sporadic ALS cases, which we primarily attribute to SOD1 gene status. Our data demonstrate co-deposition of p62 with mutant and wild-type disSOD1 and phosphorylated TDP-43 in familial and sporadic ALS spinal cord motor neurons, consistent with attempts by p62 to mitigate SOD1 and TDP-43 deposition. Wild-type SOD1 and TDP-43 co-deposition was also frequently observed in ALS cases lacking SOD1 mutations. Finally, alterations to the subcellular localization of the three proteins were tightly correlated, suggesting close relationships between the regulatory mechanisms governing the subcellular compartmentalization of these proteins. Our study is the first to profile spatial relationships between SOD1, TDP-43 and p62 pathologies in post-mortem spinal cord motor neurons of ALS patients, previously only studied in vitro. Our findings suggest interactions between these three key ALS-linked proteins are likely to modulate the formation of their respective proteinopathies, and perhaps the rate of motor neuron degeneration, in ALS patients.