Arjunolic acid, a triterpenoid saponin, ameliorates arsenic-induced cyto-toxicity in hepatocytes

Arsenic is a well-established environmental toxin, which damages various organs of the body. A triterpenoid saponin, arjunolic acid (AA) has been isolated from the bark of Terminalia arjuna. The present study was conducted to investigate the preventive role of AA against arsenic-induced cytotoxicity in isolated murine hepatocytes. Sodium arsenite (NaAsO₂) was chosen as the source of arsenic. Incubation of the hepatocytes with NaAsO₂ (1mM) for 2 h caused reduction in the cell viability and activities of the intracellular enzymatic as well as non-enzymatic antioxidants. Treatment of NaAsO₂ enhanced lipid peroxidation and also increased the activities of the membrane leakage enzymes. Administration of AA (100 μg/ml) before and with the toxin almost normalized the altered activities of antioxidant indices. AA possesses free radical scavenging activity and could enhance the cellular anti-oxidant capability against NaAsO₂-induced cyto-toxicity. The cytoprotective activity of AA was found to be comparable to that of a known antioxidant, vitamin C. Experimental results, therefore, suggest that AA protects arsenic-induced cytotoxicity in murine hepatocytes.     

Cisplatin‐Induced Testicular Toxicity in Rats: The Protective Effect of Arjunolic Acid

In the present study, the effect of arjunolic acid on testicular damage induced by intraperitoneal injection of rats with 7 mg/kg cisplatin was studied. Cisplatin induced a significant reduction in testicular weights, plasma testosterone, and testicular reduced glutathione levels in addition to a significant elevation of testicular malondialdehyde levels and testicular gene expressions of inducible nitric oxide synthase (iNOS), tumor necrosis factor‐α (TNF‐α), and p38 mitogen‐activated protein kinase (MAPK) when compared with the control group (p < 0.05). Lower tubular diameters and depletion of germ cells and irregular small seminiferous tubules with Sertoli cells only were observed in the cisplatin group. Arjunolic acid administration significantly corrected the changes in both biochemical and histopathological parameters. Arjunolic acid plays a significant protective role against cisplatin‐induced testicular injury by attenuating oxidative stress parameters along with downregulation of iNOS, TNF‐α, and p38‐MAPK testicular expressions.     

Resveratrol in cardioprotection: a therapeutic promise of alternative medicine

Resveratrol, a polyphenol phytoalexin, possesses diverse biochemical and physiological actions, including estrogenic, antiplatelet, and anti-inflammatory properties. Several recent studies determined the cardioprotective abilities of resveratrol. Both in experiments (acute) and in chronic models, resveratrol attenuates myocardial ischemic reperfusion injury, atherosclerosis, and reduces ventricular arrhythmias. It appears that resveratrol-mediated cardioprotection is achieved through the preconditioning effect (the best yet devised method of cardioprotection), rather than direct protection. Thus, resveratrol likely fulfills the definition of a pharmacological preconditioning compound and gives hope to the therapeutic promise of alternative medicine.     

Arjunolic acid ameliorates reactive oxygen species via inhibition of p47phox-serine phosphorylation and mitochondrial dysfunction

Impaired cardiovascular function during acute myocardial infarction (MI) is partly associated with recruitment of activated polymorphonuclear neutrophils. The protective role of arjunolic acid (AA; 2,3,23-trihydroxy olean-12-en-28-oic acid) is studied in the modulation of neutrophil functions in vitro by measuring the reactive oxygen species (ROS) generation. Neutrophils were isolated from normal and acute MI mice to find out the efficacy of AA in reducing oxidative stress. Stimulation of neutrophils with phorbol-12-myristate-13-acetate (PMA) resulted in an oxidative burst of superoxide anion (O₂⁻) and enhanced release of lysosomal enzymes. The treatment of neutrophils with PMA induced phosphorylation of Ser345 on p47^phox, a cytosolic component of NADPH oxidase. Furthermore, we observed activated ERK induced phosphorylation of Ser345 in MI neutrophils. Treatment with AA significantly inhibited the phosphorylation of P47^phox and ERK in the stimulated controls and MI neutrophils. Oxidative phosphorylation activities in MI cells were lower than in control, while the glycolysis rates were elevated in MI cells compared to the control. In addition, we observed AA decreased intracellular oxidative stress and reduced the levels of O₂⁻ in neutrophils. This study therefore identifies targets for AA in activated neutrophils mediated by the MAPK pathway on p47^phox involved in ROS generation.     

Protective effect of arjunolic acid against arsenic-induced oxidative stress in mouse brain

Arsenic, a notoriously poisonous metalloid, is ubiquitous in the environment, and it affects nearly all organ systems of animals including humans. The present study was designed to investigate the preventive role of a triterpenoid saponin, arjunolic acid against arsenic-induced oxidative damage in murine brain. Sodium arsenite was selected as a source of arsenic for this study. The free-radical-scavenging activity and the in vivo antioxidant power of arjunolic acid were determined from its 2,2-diphenyl-1-picryl hydrazyl radical scavenging ability and ferric reducing/antioxidant power assay, respectively. Oral administration of sodium arsenite at a dose of 10 mg/kg body weight for 2 days significantly decreased the activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione-S-transferase, glutathione reductase and glutathione peroxidase, the level of cellular metabolites, reduced glutathione, total thiols and increased the level of oxidized glutathione. In addition, it enhanced the levels of lipid peroxidation end products and protein carbonyl content. Treatment with arjunolic acid at a dose of 20 mg/kg body weight for 4 days prior to arsenic administration almost normalized above indices. Histological findings due to arsenic intoxication and arjunolic acid treatment supported the other biochemical changes in murine brains. Results of 2,2-diphenyl-1-picryl hydrazyl radical scavenging and ferric reducing/antioxidant power assays clearly showed the in vitro radical scavenging as well as the in vivo antioxidant power of arjunolic acid, respectively. The effect of a well-established antioxidant, vitamin C, has been included in the study as a positive control. Combining all, results suggest that arjunolic acid possessed the ability to ameliorate arsenic-induced oxidative insult in murine brain and is probably due to its antioxidant activity.     

Effect of rosmarinic acid on inhibition of gentamicin induced nephrotoxicity in rats

The present investigation reports the effect of rosmarinic acid (RA), an antioxidant on gentamicin sulphate (GS)-induced renal oxidative damage in rats. Rosmarinic acid (RA) has been demonstrated to have antioxidant, free radical scavenger and anti-inflamatory effects. Twenty-eight Sprague-Dawley rats were divided in to four equal groups as follows: group 1 (control), group 2 (GS 100 mg/kg/d ip), group 3 (GS 100 mg/kg/d ip + RA 50 mg/kg/d) and group 4 (GS 100 mg/kg/d ip + RA 100 mg/kg/d). Treatments were administrated once daily for 12 days. After 12 days 24 h urine was collected, blood was sampled and kidneys were removed. Serum and kidney tissue MDA assessed by thiobarbituric acid. Kidney paraffin sections (5 μm thickness) from the left kidney stained with periodic acid Schiff. Tubular necrosis was studied semiquantitatively and glomerular volume and volume density of proximal convoluted tubule (PCT) estimated stereologically. Kidney homogenize were prepared from right kidney. Serum creatinine, urea and kidney antioxidant enzymes activity were assessed by special kits. Data were compared by SPSS 13 software and Mann–Whitney test at p < 0.05. Co treatment of GS and RA (High dose) significantly decreased serum creatinine, MDA, urea, tubular necrosis (p < 0.05) and increase renal GSH, GPX, CAT, SOD, volume density of PCT and creatinine clearance significantly in comparison with GS group (p < 0.05). Treatment with RA (high dose) maintained serum creatinine, volume density of PCT, renal GSH, GPX, SOD and MDA as the same level as control group significantly (p < 0.05). In conclusion, RA alleviates GS nephrotoxicity via antioxidant activity, increase of renal GSH content and increase of renal antioxidant enzymes activity.     

Dimerumic acid protected oxidative stress-induced cytotoxicity in isolated rat hepatocytes

Dimerumic acid (DMA) is contained in Monascus anka and Monascus pilosus fermented products. The purpose of this study was to evaluate the effect of DMA against salicylic acid (SA)- and tert-butylhydroperoxide (t-BHP)-induced oxidative stress and cytotoxicity in the liver, using rat liver microsomes and isolated rat hepatocytes. DMA was extracted from monascus-garlic-fermented extract using M. pilosus. In rat liver microsomes, 1 microM DMA decreased SA-induced lipid peroxidation but did not affect the production of the oxidative metabolite of SA via CYP. In isolated rat hepatocytes, 1 microM DMA decreased SA-induced lipid peroxidation and chemiluminescence (CL) generation and the intracellular glutathione-reduced form/oxidized form (GSH/GSSG) ratio in the presence of 1 microM DMA was higher than that without DMA; however, 100 microM DMA suppressed the leakage of lactate dehydrogenase (LDH). On the other hand, t-BHP-induced lipid peroxidation, CL generation, and LDH leakage were prevented by 100 microM DMA. Thus, DMA showed an antioxidative effect in hepatocytes and protected against hepatotoxicity by suppressing oxidative stress without affecting CYP enzymes.     

Ameliorative synergistic therapeutic effect of gallic acid and albendazole against Trichinella spiralis muscular phase infection and assessment of their effects on hepatic and cardiac tissues in male mice

Trichinellosis is a serious food-borne parasitic disease with serious community health effects, mainly causing muscle damage with no recent approved treatment. This study aimed to assess the therapeutic effect of gallic acid (GA) as a potent antioxidant against the encysted phase of Trichinella spiralis in male (BALB/c) mice alone or combined with albendazole (ALB) and to detect their synergistic effects on the histology and ultrastructure of skeletal and cardiac muscles and some biochemical blood analyses. Forty male mice were randomly divided into five groups (8 mice/group). 1^st group: the negative control received only distilled water, 2^nd group: the positive control (infected control group without treatment), 3^rd group: infected group plus treatment with ALB (50 mg Kg⁻¹ orally), and 4^th group: infected group and then treated with GA (30 mg Kg⁻¹ orally) and finally 5^th infected group treated with a combination of both ALB and GA. Aspartate and Alanine aminotransferase, Lactate dehydrogenase, alkaline phosphatase, C-reactive protein, Interleukin-4 and Creatine kinase were used as biochemical markers of hepatic and cardiac toxicity and inflammation. Malondialdehyde level, catalase, superoxide dismutase, and glutathione peroxidase were evaluated in heart tissue homogenates beside histological and ultra-structural examination of heart and skeletal muscles beside parasitological analyses. Results showed that the reduction % of Trichinella sp. larvae g⁻¹ in muscles of the group treated with the combination of GA and ALB showed overall reduction percentages. Oral administration of 30 mg kg¹ of GA led to infection reduction of T. spiralis than ALB treated group. Both administration of ALB beside GA showed the best treatment group that resulted in high infection reduction besides amelioration of both biochemical markers and restoration of histological and ultrastructures to normal state. In conclusion, GA is highly effective against T. spiralis which could be a promising alternative antioxidant drug and the GA effect was higher in the case of combination with ALB. This experiment provides a basis for further exploration of potent activities of other antioxidants against different phases of T. spiralis and the reduction of any health hazards prospectively.     

Arjunolic acid: beneficial role in type 1 diabetes and its associated organ pathophysiology

Abstract

In this review article, we describe the most recent development of the beneficial effect of arjunolic acid (AA) in reducing type 1 diabetic pathophysiology. Diabetic mellitus is a serious and growing health problem worldwide. Increasing evidence suggest that oxidative stress plays a pivotal role in the pathogenesis of diabetes and its associated complications. Use of antioxidant supplements as a complimentary therapeutic approach in diabetes has, therefore, been seriously considered worldwide. AA, a natural pentacyclic triterpenoid saponin, is well known for various biological functions including antioxidant activity. It could prevent the increased production of ROS, RNS, AGEs, and the 8OHdG/2dG ratio and increase the intracellular antioxidant defence system. Signal transduction studies showed that AA could prevent hyperglycaemia induced activation of MAPKs, PKC, NF-κB signalling cascades and apoptotic cell death. Combining, AA supplements could be regarded as beneficial therapeutics in the treatment of diabetes and its associated complications.     

Impaired redox signaling and mitochondrial uncoupling contributes vascular inflammation and cardiac dysfunction in type 1 diabetes: Protective role of arjunolic acid

Vascular inflammation and cardiac dysfunction are the leading causes of mortality and morbidity among the diabetic patients. Type 1 diabetic mellitus (T1DM) is associated with increased cardiovascular complications at an early stage of the disease. The purpose of the present study was to explore whether arjunolic acid (AA) plays any protective role against cardiovascular complications in T1DM and if so, what molecular pathways it utilizes for the mechanism of its protective action. Streptozotocin (STZ) was used to induce T1DM in experimental rats. Alteration in plasma lipid profile and release of membrane bound enzymes like LDH (lactate dehydrogenase) and CK (creatine kinase) established the association of hyperlipidemia and cell membrane disintegration with hyperglycemia. Hyperglycemia altered the levels of oxidative stress related biomarkers, decreased the intracellular NAD and ATP concentrations. Hyperglycemia-induced enhanced levels of VEGF, ICAM-1, MCP-1 and IL-6 in the plasma of STZ treated animals indicate vascular inflammation in T1DM. Histological studies and FACS analysis revealed that hyperglycemia caused cell death mostly via the apoptotic pathway. Investigating molecular mechanism, we observed NF-κB and MAPKs (p38 and ERK1/2) activations, mitochondrial membrane depolarization, cytochrome C release, caspase 3 activation and PARP cleavage in apoptotic cell death in the diabetic cardiac tissue. Treatment with AA (20 mg/kg body weight) reduced hyperglycemia, membrane disintegration, oxidative stress, vascular inflammation and prevented the activation of oxidative stress induced signaling cascades leading to cell death. Results suggest that AA possesses the potential to be a beneficial therapeutic agent in diabetes and its associated cardiac complications.     

A polyphenolic flavonoid glabridin: Oxidative stress response in multidrug-resistant Staphylococcus aureus

Glabridin a polyphenolic flavonoid from Glycyrrhiza glabra is known to possess several therapeutic properties. In the present study, we report for the first time the in vitro antibacterial activity (MIC values ranging from 3.12 to 25 μg/mL) of glabridin against multidrug-resistant clinical isolates of S. aureus by inducing oxidative stress. Increased levels of H₂O₂ and NO were observed in a dose-dependent manner after treatment of glabridin that further affected macromolecules such as DNA, lipids, and proteins. Surprisingly, glabridin was found to possess antioxidant properties when used at lower concentrations using three different methods including DPPH, FRAP, and SOD assays. These observations were further validated through the expression analysis of oxidative stress-responsive genes using qRT-PCR wherein glabridin was observed to up- and down-regulate these genes at lower and higher concentrations, respectively. In in vitro combination experiments, glabridin was found to reduce the MIC of different antibiotics such as norfloxacin, oxacillin, and vancomycin by up to 4-fold, while the MIC of glabridin itself was found to be reduced by up to 8-fold in the presence of antibiotics. A synergistic interaction was observed between norfloxacin and glabridin when used in combination against multidrug-resistant clinical isolate SA 4627 of Staphylococcus aureus at much lower concentrations, indicating the suitability of glabridin in combination therapy.     

Antioxidant responses of Propylaea japonica (Coleoptera: Coccinellidae) exposed to high temperature stress

Temperature is one of the most important environmental factors, and is responsible for a variety of physiological stress responses in organisms. Induced thermal stress is associated with elevated reactive oxygen species (ROS) generation leading to oxidative damage. The ladybeetle, Propylaea japonica (Thunberg) (Coleoptera: Coccinellidae), is considered a successful natural enemy because of its tolerance to high temperatures in arid and semi-arid areas in China. In this study, we investigated the effect of high temperatures (35, 37, 39, 41 and 43 °C) on the survival and activities of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), peroxidases (POD), glutathione-S-transferases (GST), and total antioxidant capacity (TAC) as well as malondialdehyde (MDA) concentrations in P. japonica adults. The results indicated that P. japonica adults could not survive at 43 °C. CAT, GST and TAC were significantly increased when compared to the control (25 °C), and this played an important role in the process of antioxidant response to thermal stress. SOD and POD activity, as well as MDA, did not differ significantly at 35 and 37 °C compared to the control; however, there were increased levels of SOD, POD and MDA when the temperature was above 37 °C. These results suggest that thermal stress leads to oxidative stress and antioxidant enzymes play important roles in reducing oxidative damage in P. japonica adults. This study represents the first comprehensive report on the antioxidant defense system in predaceous coccinellids (the third trophic level). The findings provide useful information for predicting population dynamics and understanding the potential for P. japonica as a natural enemy to control pest insects under varied environmental conditions.     

Cryopreservation of epididymal cat spermatozoa: effects of in vitro antioxidative enzymes supplementation and lipid peroxidation induction

Reactive oxygen species and lipid peroxidation reaction, causes of sperm damage, can be diminished by action of antioxidative enzymes. This study aimed to investigate effects of (1) the antioxidative enzymes; catalase, glutathione peroxidase and superoxide dismutase, on epipididymal cat sperm quality and (2) the lipid peroxidation reaction induced by a transition metal (ferrous ion (II); Fe²⁺) on sperm quality during the cryopreservation process. Epididymal spermatozoa harvested from 39 male cats were pooled and divided into 13 aliquots (n = 13). Each aliquot was resuspended with either a Tris egg yolk extender I (control; EE-I), or the Tris egg yolk extender I supplemented with 200 U/mL catalase (EE-CAT), or 10 U/mL glutathione peroxidase (EE-GPx), or 600 U/mL superoxide dismutase (EE-SOD), and then cryopreserved. After thawing, each sperm sample was subdivided into two groups; with and without lipid peroxidation induction (EE-I plus Fe²⁺, EE-CAT plus Fe²⁺, EE-GPx plus Fe²⁺ and EE-SOD plus Fe²⁺). Subjective sperm motility, membrane, and acrosome integrity were evaluated at the time of collection, after cooling, and at 0, 2, 4, and 6 h after thawing. Motility patterns assessed by computer-assisted sperm analysis (CASA), mitochondrial activity, and DNA integrity were evaluated during post-thaw incubation, whereas percentage of lipid peroxidation was detected at 0 and 6 h after thawing. The results demonstrate that catalase supplementation reduced linear motility and subjective motility immediately and 2 h after thawing (P < 0.05). Catalase supplementation, however, improved DNA integrity at 4 h (P < 0.05). Supplementation with glutathione peroxidase, compared to the control group, had a statistically significant positive effect on subjective motility at 0 and 6 h, linear motility at 6 h, mitochondrial activity at 6 h, membrane integrity at 2 and 6 h, and DNA integrity at 4 h after thawing. Although superoxide dismutase had a positive effect on sperm membrane integrity at 2 h after thawing (P < 0.05), it significantly reduced membrane integrity after cooling, linear motility at thawing, and acrosome integrity at 2 h after thawing. None of the three selected antioxidative enzymes significantly influenced acrosome integrity and none reduced the level of lipid peroxidation. Furthermore, induction of the lipid peroxidation reaction by Fe²⁺ negatively affected most of the sperm quality parameters, i.e., motility and DNA integrity, during post-thaw sperm incubation (P < 0.05). After thawing, there were, however, no significant differences between the control plus Fe²⁺ and the antioxidative enzymes supplementation plus Fe²⁺ groups. We can conclude that (1) glutathione peroxidase exhibits positive effects on post-thaw epididymal cat spermatozoa; but (2) none among the selected antioxidative enzymes could improve all sperm quality parameters; and (3) the lipid peroxidation reaction may be one cause of post-thaw epididymal sperm damage in cats, but the concentrations of antioxidative enzymes used in this study could not protect cat spermatozoa from lipid peroxidation induction.     

Molecular mechanisms of a novel selenium-based complementary medicine which confers protection against hyperandrogenism-induced polycystic ovary

The objective was to evaluate ovarian functionality and oxidative response in hyperandrogenism-induced polycystic ovary (PCO) and the protective effects of immunomodulator drug (IMOD), an electromagnetically-treated, selenium-based, herbal medicine. Daily oral administration of letrozole (1 mg/kg) for 21 consecutive days induced ovarian cysts in female rats. An effective dose of IMOD (30 mg/kg per day) was given intraperitoneally for 21 days. Biomarkers of ovarian function, serum concentrations of estradiol, progesterone, testosterone, and ovarian prostaglandin-E (PGE), were analyzed. To determine the role of oxidative stress (OS) in hyperandrogenism-induced PCO, concentrations of cellular lipid peroxidation (LPO), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), peroxynitrite (ONOO), and tumor necrosis factor (TNF)-α as a marker of inflammation and apoptosis were measured in serum and ovaries. Letrozole-induced PCO resulted in significant increases in concentrations of lipid peroxidation and peroxynitrite in serum and ovary, but significantly decreased superoxide dismutase, catalase, and glutathione peroxidase. Serum concentrations of testosterone and TNF-α, and ovarian prostaglandin-E were increased (P < 0.001) in animals with cysts versus control, whereas estradiol and progesterone were decreased (P < 0.01 and P < 0.001, respectively). When compared with controls, letrozole induced irregular cycles and PCO characterized by a high incidence of subcapsular ovarian cysts with a diminished granulosa cell layer, luteinized granulosa cells in the cyst wall, significantly more atretic preantral and antral follicles, and absence of CL. There were almost no intact primary, secondary, and tertiary follicles in PCO rats. All end points assessed were significantly improved by IMOD and reached close to normal levels. In conclusion, the present study provided evidence that toxic free radicals and TNF-α were involved in the pathogenesis of PCO; furthermore, IMOD prevented ovarian histopathologic, endocrine, and biochemical alterations induced by hyperandrogenism.     

Micropropagation of gerbera: lipid peroxidation and antioxidant enzyme activities during acclimatization process

Gerbera jamesonii H. Bolus ex Hook (Family: Asteraceae) has been successfully acclimatized from temperate to subtropical North Indian plains of Lucknow through in vitro propagation. Flower heads were collected from greenhouse, segmented into 4–16 pieces and cultured in Murashige and Skoog’s medium (MS) (Physiol Plant 15:472–497, 1962) supplemented with 2.87 μM indole-3-acetic acid (IAA) and 8.88 μM N⁶-benzyladenine (BA) for shoot regeneration. Shoots were subcultured on growth regulator free MS medium. Apical shoot meristems from in vitro plantlets of gerbera were tested in MS medium with different combination of cytokinins [BA, kinetin, and thidiazuron (TDZ)] alongwith 2.68 μM 1-naphthaleneacetic acid (NAA) for shoot multiplication. The optimum results were obtained with 8.88 μM BA. Regenerated plants with well-established root system were transferred to pots containing soil and sand (1:1 v/v) and were kept in humidity chamber with 80–90% relative humidity for 0, 5, 10, 15, 20, and 25 days before they were transferred to field (during October, 2005 to February, 2006). Survival percentage was higher when regenerated plantlets were kept under humidity chamber for 15 days. An attempt was made to obtain basic information on different biochemical changes during acclimatization process of in vitro raised plantlets. Increased lipid peroxidation and high H₂O₂ content in early stages of acclimatization process reflected a similar process of oxidative stress. Our work suggests that tissue-cultured plants develop antioxidant enzymatic protective system which determine the ability to survive in oxidative stress and up regulation of these enzymes would help to reduce the built up of reactive oxygen species (ROS).     

A novel procedure for the assessment of the antioxidant capacity of food components

Carbonylation, an oxidative modification of the amino group of arginine and lysine residues caused by reactive oxygen species, has emerged as a new type of oxidative damage. Protein carbonylation has been shown to exert adverse effects on various protein functions. Recently, the role of food components in the attenuation of oxidative stress has been the focus of many studies. Most of these studies focused on the chemical properties of food components. However, it is also important to determine their effects on protein functions via post-translational modifications. In this study, we developed a novel procedure for evaluating the antioxidant capacity of food components. Hydrogen peroxide (H₂O₂)-induced protein carbonylation in HL-60 cells was quantitatively analyzed by using fluorescent dyes (Cy5–hydrazide dye and IC3–OSu dye), followed by sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS–PAGE) and fluorescence determination. Among a panel of food components tested, quinic acid, kaempferol, saponin, squalene, trigonelline, and mangiferin were shown to be capable of suppressing protein carbonylation in HL-60 cells. Our results demonstrated that this fluorescence labeling/SDS–PAGE procedure allows for the detection of oxidative stress-induced protein carbonylation with high sensitivity and quantitative accuracy. This method should be useful for the screening of new antioxidant food components as well as the analysis of their suppression mechanism.     

Antioxidant responses of the pest natural enemy Hylyphantes graminicola (Araneae: Linyphiidae) exposed to short-term heat stress

Temperature is a critical abiotic factor that causes physiological changes in arthropods. However, little is known about the effect of heat stress on the antioxidant responses of Araneae species. Hylyphantes graminicola is a dominant predator in many cropping systems in China. In the present study, the effect of short-term heat stress (36, 38, 40 or 42 °C) on the reactive oxygen species (ROS) levels, the activities of antioxidant enzymes (superoxide dismutase [SOD], catalase [CAT], peroxidases [POD] and glutathione-S-transferases GST]), total antioxidant capacity (TAC), malondialdehyde (MDA) concentrations and survival of H. graminicola spiderlings and adults were investigated. The results showed that H. graminicola adults had a significantly higher survival rate compared to spiderlings at 40 °C. The heat stress increased ROS contents in H. graminicola. The SOD, CAT, POD and GST activities increased in spiderlings and adults under heat stress. These data suggest a defensive function for these enzymes in alleviating oxidative damage. Specifically, SOD plays a key role in reducing the high level of superoxide radicals in spiderlings and adults. Moreover, the POD and CAT capabilities for scavenging H₂O₂ in spiderlings were similar, and CAT may play a more important role than POD in scavenging H₂O₂ in adults at 42 °C. The spiderling TAC increased significantly at 40 and 42 °C, and the adult TAC was stable at 36–40 °C but decreased at 42 °C. These data suggest that TAC was insufficient in H. graminicola adults under more severe stress conditions. These results further our understanding of the physiological response of Araneae species exposed to heat stress.