Showing papers on "Malondialdehyde published in 2011"
TL;DR: The acute toxicity and oxidative effects of nano-scale titanium dioxide, zinc oxide and their bulk counterparts in zebrafish were studied and showed that after the illumination for 96 h, the quantities of ·OH in the NP suspensions were much higher than ones in the bulk particles suspensions.
495 citations
TL;DR: The CFH polymorphism H402, which is strongly associated with AMD, markedly reduces the ability of CFH to bind MDA, indicating a causal link to disease aetiology.
Abstract: Oxidative stress and enhanced lipid peroxidation are linked to many chronic inflammatory diseases, including age-related macular degeneration (AMD). AMD is the leading cause of blindness in Western societies, but its aetiology remains largely unknown. Malondialdehyde (MDA) is a common lipid peroxidation product that accumulates in many pathophysiological processes, including AMD. Here we identify complement factor H (CFH) as a major MDA-binding protein that can block both the uptake of MDA-modified proteins by macrophages and MDA-induced proinflammatory effects in vivo in mice. The CFH polymorphism H402, which is strongly associated with AMD, markedly reduces the ability of CFH to bind MDA, indicating a causal link to disease aetiology. Our findings provide important mechanistic insights into innate immune responses to oxidative stress, which may be exploited in the prevention of and therapy for AMD and other chronic inflammatory diseases.
479 citations
TL;DR: High fat diet-induced obesity is accompanied by increased hepatic, heart, and renal tissues oxidative stress, which is characterized by reduction in the antioxidant enzymes activities and glutathione levels, that correlate with the increase in MDA and PCO levels in most tissues.
Abstract: Background: Obesity has become a leading global health problem owing to its strong association with a high incidence of diseases. Aim: To induce rat obesity using high fat diet (HFD) and to estimate oxidative stress markers in their liver, heart and kidney tissues in order to shed the light on the effect of obesity on these organs. Materials and methods: Sixty white albino rats weighing 150-200 g were randomly divided into two equal groups; group I: received high fat diet for 16 weeks, and group II (control group): received only normal diet (rat chow) for 16 weeks. Blood samples were taken for measurement of lipid profile, tissue samples from liver, heart and kidney were taken for determination of malondialdehyde (MDA), protein carbonyl (PCO), reduced glutathione (GSH) levels, and the activities of glutathione S- transferase (GST) glutathione peroxidase (GPx), catalase (CAT) and paraoxonase1 (PON1) enzymes. Results: Data showed that feeding HFD diet significantly increased final body weight and induced a state of dyslipideamia. Also our results showed a significant increase MDA and PCO levels in the hepatic, heart and renal tissues of obese rats, as well as a significant decrease in the activity of GST, GPx and PON 1 enzymes. On the other hand CAT enzyme activity showed significant decrease only in renal tissues of obese rats with non significant difference in hepatic and heart tissues. GSH levels showed significant decrease in both renal and hepatic tissues of obese animals and significant increase in their heart tissues. Correlation studies in obese animals showed a negative correlation between MDA and PCO tissue levels and the activities of GPx, GST and PON1 in all tissues and also with CAT enzyme activity in renal tissues. Also a negative correlation was detected between MDA & PCO tissues levels and GSH levels in both hepatic and renal tissues. While positive correlation was found between them and GSH levels in heart tissues. Conclusion: High fat diet-induced obesity is accompanied by increased hepatic, heart, and renal tissues oxidative stress, which is characterized by reduction in the antioxidant enzymes activities and glutathione levels, that correlate with the increase in MDA and PCO levels in most tissues. This may probably contribute to the additional progression of obesity related problems.
402 citations
TL;DR: The current knowledge on DNA damage induced by endogenously produced reactive aldehydes in relation to the pathophysiology of human diseases is discussed.
Abstract: DNA damage plays a major role in various pathophysiological conditions including carcinogenesis, aging, inflammation, diabetes and neurodegenerative diseases. Oxidative stress and cell processes such as lipid peroxidation and glycation induce the formation of highly reactive endogenous aldehydes that react directly with DNA, form aldehyde-derived DNA adducts and lead to DNA damage. In occasion of persistent conditions that influence the formation and accumulation of aldehyde-derived DNA adducts the resulting unrepaired DNA damage causes deregulation of cell homeostasis and thus significantly contributes to disease phenotype. Some of the most highly reactive aldehydes produced endogenously are 4-hydroxy-2-nonenal, malondialdehyde, acrolein, crotonaldehyde and methylglyoxal. The mutagenic and carcinogenic effects associated with the elevated levels of these reactive aldehydes, especially, under conditions of stress, are attributed to their capability of causing directly modification of DNA bases or yielding promutagenic exocyclic adducts. In this review, we discuss the current knowledge on DNA damage induced by endogenously produced reactive aldehydes in relation to the pathophysiology of human diseases.
244 citations
TL;DR: Dietary inorganic nitrate supplementation is strongly protective in this model of renal and cardiovascular disease and future studies will reveal if nitrate contributes to the well-known cardioprotective effects of a diet rich in vegetables.
Abstract: Aims Reduced bioavailability of endogenous nitric oxide (NO) is a central pathophysiological event in hypertension and other cardiovascular diseases. Recently, it was demonstrated that inorganic nitrate from dietary sources is converted in vivo to form nitrite, NO, and other bioactive nitrogen oxides. We tested the hypothesis that dietary inorganic nitrate supplementation may have therapeutic effects in a model of renal and cardiovascular disease.
Methods and results Sprague–Dawley rats subjected to unilateral nephrectomy and chronic high-salt diet from 3 weeks of age developed hypertension, cardiac hypertrophy and fibrosis, proteinuria, and histological as well as biochemical signs of renal damage and oxidative stress. Simultaneous nitrate treatment (0.1 or 1 mmol nitrate kg−1 day−1), with the lower dose resembling the nitrate content of a diet rich in vegetables, attenuated hypertension dose-dependently with no signs of tolerance. Nitrate treatment almost completely prevented proteinuria and histological signs of renal injury, and the cardiac hypertrophy and fibrosis were attenuated. Mechanistically, dietary nitrate restored the tissue levels of bioactive nitrogen oxides and reduced the levels of oxidative stress markers in plasma (malondialdehyde) and urine (Class VI F2-isoprostanes and 8-hydroxy-2-deoxyguanosine). In addition, the increased circulating and urinary levels of dimethylarginines (ADMA and SDMA) in the hypertensive rats were normalized by nitrate supplementation.
Conclusion Dietary inorganic nitrate is strongly protective in this model of renal and cardiovascular disease. Future studies will reveal if nitrate contributes to the well-known cardioprotective effects of a diet rich in vegetables.
238 citations
TL;DR: Results demonstrate that inhibition of PPARα functions may increase susceptibility to high fat-induced NASH, with increased steatosis, oxidative stress, and inflammation observed in Ppara-null mice fed a HFD.
Abstract: Emerging evidence suggests that the lack of PPARα enhances hepatic steatosis and inflammation in Ppara-null mice when fed a high-fat diet (HFD). Thus, the aim of this study was to determine whether Ppara-null mice are more susceptible to nonalcoholic steatohepatitis (NASH) than their wild-type (WT) counterparts following short-term feeding with a HFD. Age-matched male WT and Ppara-null mice were randomly assigned to consume ad libitum a standard Lieber-DeCarli liquid diet (STD) (35% energy from fat) or a HFD (71% energy from fat) for 3 wk. Liver histology, plasma transaminase levels, and indicators of oxidative/nitrosative stress and inflammatory cytokines were evaluated in all groups. Levels of lobular inflammation and the NASH activity score were greater in HFD-exposed Ppara-null mice than in the other 3 groups. Biochemical analysis revealed elevated levels of ethanol-inducible cytochrome P450 2E1 and TNFα accompanied by increased levels of malondialdehyde as well as oxidized and nitrated proteins in Ppara-null mice. Elevated oxidative stress and inflammation were associated with activation of c-Jun-N-terminal kinase and p38 kinase, resulting in increased hepatocyte apoptosis in Ppara-null mice fed a HFD. These results, with increased steatosis, oxidative stress, and inflammation observed in Ppara-null mice fed a HFD, demonstrate that inhibition of PPARα functions may increase susceptibility to high fat-induced NASH.
225 citations
TL;DR: In this article, the authors evaluated the protection potential of acetyl-l-carnitine, DL-α-lipoic acid and silymarin against cisplatin-induced myocardial injury.
205 citations
TL;DR: This study shows for the first time in an in vivo model of diabetes that GLO-I overexpression reduces hyperglycemia-induced levels of carbonyl stress, AGEs, and oxidative stress.
200 citations
TL;DR: The neuroprotective effect of resveratrol pretreatment was identified and the Nrf2/ARE signaling mechanism after focal cerebral I/R injury in rats was elucidated to elucidate the NRF2-related factor 2/antioxidant response element signaling mechanism.
Abstract: Oxidative stress damage plays a vital role in cerebral ischemia/reperfusion (I/R) pathogenesis. The nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway can be activated by pharmacological and dietary means to attenuate cellular oxidative stress. Resveratrol, a plant-derived polyphenolic compound, has antioxidant property. Recent studies have demonstrated that resveratrol has protective effects against cerebral I/R injury. However, little is known about its mechanism. Hence, this study identified the neuroprotective effect of resveratrol pretreatment and elucidate the Nrf2/ARE signaling mechanism after focal cerebral I/R injury in rats. Adult male Sprague–Dawley rats were randomly assigned to sham-operated group, ischemia/reperfusion physiological saline-treated group, and ischemia/reperfusion resveratrol-pretreatmented (15 and 30 mg/kg) groups. Rats were pretreatmented with resveratrol or physiological saline of corresponding volume administered intraperitoneally for 7 days before surgery and 30 min before middle cerebral artery occlusion. At 24 h after reperfusion, neurological score, infarct volume, and brain water content were assessed. Oxidative stress was evaluated by malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity. Pathological changes of brain tissue were observed by HE staining. RT-PCR and Western blot analysed the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1). TUNEL staining detected apoptotic cells. The protein expression of Caspase-3 were studied by immunohistochemistry. Resveratrol pretreatment significantly ameliorated neurological scores, reduced infarct volume and brain water content, decreased MDA levels, restored the SOD activity, upregulated the protein and mRNA expression of Nrf2 and HO-1, downregulated the protein expression of caspase-3. TUNEL-positive cells significantly decreased compared with the physiological saline-treated group. HE staining also showed that resveratrol significantly improved neuronal injury. These results showed that resveratrol pretreatment had neuroprotective effects on cerebral I/R injury. This neuroprotective effect is likely exerted by upregulated expression of transcription factor Nrf2 and HO-1 to ameliorate oxidative damage, decreased the protein expression of caspase-3. Our finding is important for understanding the neuroprotective mechanism of resveratrol and promoting its clinical therapeutic utility.
197 citations
TL;DR: Pretreatment with date palm fruit extract restored the liver damage induced by dimethoate, as revealed by inhibition of hepatic lipid peroxidation, amelioration of SOD, GPx and CAT activities and improvement of histopathology changes.
191 citations
TL;DR: Sarcoidosis patients might benefit from the use of antioxidants, such as quercetin, to reduce the occurring oxidative stress as well as inflammation, indicated by the increased total plasma antioxidant capacity.
TL;DR: An increase in dairy intake attenuates oxidative and inflammatory stress in metabolic syndrome andificantly reduced waist circumference and trunk fat in subjects with metabolic syndrome.
TL;DR: The findings indicated that heat stress-induced inhibition in growth and chlorosis was associated with decrease in leaf water status and elevation of oxidative stress, which could partly be prevented by exogenous application of ASC.
Abstract: The rising temperatures (>35°C) are proving detrimental to summer-sown mungbean genotypes that experience inhibition of vegetative and reproductive growth. In the present study, the mungbean plants growing hydroponically at varying temperatures of 30/20°C (control), 35/25, 40/30, and 45/35°C (as day/night 12 h/12 h) with (50 μM) or without ascorbic acid (ASC) were investigated for effects on growth, membrane damage, chlorophyll loss, leaf water status, components of oxidative stress, and antioxidants. The ASC-treated plants showed significant improvement in germination and seedling growth especially at 40/30 and 45/35°C. The damage to membranes, loss of water, decrease in cellular respiration, and chlorophyll were significantly prevented by ASC treatment to plants growing at these temperatures. The oxidative stress measured as malondialdehyde and hydrogen peroxide content was observed to be significantly lower at high temperatures with ASC application. The activities of superoxide dismutase, catalase, ascorbate peroxidase, and glutathione reductase increased at 40/30°C but decreased at 45/35°C in the absence of ASC while with its application, the activities of these enzymes were appreciably resorted. Among all the antioxidants, the endogenous ASC content decreased to the greatest extent at 45/35°C grown plants indicating its vital role in affecting the response of mungbean to heat stress. Exogenously applied ASC raised its endogenous content along with that of glutathione and proline at 45/35°C. The findings indicated that heat stress-induced inhibition in growth and chlorosis was associated with decrease in leaf water status and elevation of oxidative stress, which could partly be prevented by exogenous application of ASC. Its role in imparting protection against heat stress is discussed.
TL;DR: The data of this study support a chemopreventive potential of licorice extract against liver oxidative injury and significantly reverses the increased liver hydroxyproline and serum TNF-α levels induced by CCl4 intoxication.
Abstract: Licorice has been used in Chinese folk medicine for the treatment of various disorders. Licorice has the biological capabilities of detoxication, antioxidation, and antiinfection. In this study, we evaluated the antihepatotoxic effect of licorice aqueous extract (LE) on the carbon tetrachloride (CCl4)-induced liver injury in a rat model. Hepatic damage, as reveled by histology and the increased activities of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) activities, and decreased levels of serum total protein (TP), albumin (Alb) and globulin (G) were induced in rats by an administration of CCl4 at 3 mL/kg b.w. (1:1 in groundnut oil). Licorice extract significantly inhibited the elevated AST, ALP and ALT activities and the decreased TP, Alb and G levels caused by CCl4 intoxication. It also enhanced liver super oxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), Glutathione S-transferase (GST) activities and glutathione (GSH) level, reduced malondialdehyde (MDA) level. Licorice extract still markedly reverses the increased liver hydroxyproline and serum TNF-α levels induced by CCl4 intoxication. The data of this study support a chemopreventive potential of licorice extract against liver oxidative injury.
TL;DR: Genistein is able to reverse a diabetes established condition of allodynia, oxidative stress and inflammation, ameliorates NGF content and the vascular dysfunction, thus suggesting its possible therapeutic use for diabetes complications.
TL;DR: It is thought that the evaluation of oxidative status may allow for the identification of patients at an increased risk of complications, and decreasing the levels of chronic inflammation and oxidative stress in childhood may decrease cardiovascular morbidity and mortality in adulthood.
TL;DR: The results suggest that FA protects from CCl(4)-induced acute liver injury through reduction of oxidative damage and inflammatory signaling pathways.
TL;DR: Hypoglycemic and insulin-sensitizing capability of 1% OPE were demonstrated by significant improvement of glucose tolerance as expressed in incremental area under the curve, and the mechanism for the effects of OPE showed greater potency than pure quercetin equivalent.
Abstract: Background: Quercetin derivatives in onions have been regarded as the most important flavonoids to improve diabetic status in cells and animal models. The present study was aimed to examine the hypoglycemic and insulinsensitizing capacity of onion peel extract (OPE) containing high quercetin in high fat diet/streptozotocin-induced diabetic rats and to elucidate the mechanism of its insulin-sensitizing effect. Methods: Male Sprague-Dawley rats were fed the AIN-93G diet modified to contain 41.2% fat and intraperitoneally injected with a single dose of streptozotocin (40 mg/kg body weight). One week after injection, the rats with fasting blood glucose levels above 126 mg/dL were randomly divided into 4 groups to treat with high fat diet containing 0 (diabetic control), 0.5, or 1% of OPE or 0.1% quercetin (quercetin equivalent to 1% of OPE) for 8 weeks. To investigate the mechanism for the effects of OPE, we examined biochemical parameters (insulin sensitivity and oxidative stresses) and protein and gene expressions (pro-inflammatory cytokines and receptors). Results: Compared to the diabetic control, hypoglycemic and insulin-sensitizing capability of 1% OPE were demonstrated by significant improvement of glucose tolerance as expressed in incremental area under the curve (P = 0.0148). The insulin-sensitizing effect of OPE was further supported by increased glycogen levels in liver and skeletal muscle (P < 0.0001 and P = 0.0089, respectively). Quantitative RT-PCR analysis showed increased expression of insulin receptor (P = 0.0408) and GLUT4 (P = 0.0346) in muscle tissues. The oxidative stress, as assessed by superoxide dismutase activity and malondialdehyde formation, plasma free fatty acids, and hepatic protein expressions of IL-6 were significantly reduced by 1% OPE administration (P = 0.0393, 0.0237, 0.0148 and 0.0025, respectively). Conclusion: OPE might improve glucose response and insulin resistance associated with type 2 diabetes by alleviating metabolic dysregulation of free fatty acids, suppressing oxidative stress, up-regulating glucose uptake at peripheral tissues, and/or down-regulating inflammatory gene expression in liver. Moreover, in most cases, OPE showed greater potency than pure quercetin equivalent. These findings provide a basis for the use of onion peel to improve insulin insensitivity in type 2 diabetes.
TL;DR: The positive role of OsAKR1 in abiotic stress-related reactive aldehyde detoxification pathways and its use for improvement of stress tolerance in plants is supported.
Abstract: The accumulation of toxic compounds generated by the interaction between reactive oxygen species and polyunsaturated fatty acids of membrane lipids can significantly damage plant cells. A plethora of enzymes act on these reactive carbonyls, reducing their toxicity. Based on the chromosomal localization and on their homology with other stress-induced aldo–keto reductases (AKRs) we have selected three rice AKR genes. The transcription level of OsAKR1 was greatly induced by abscisic acid and various stress treatments; the other two AKR genes tested were moderately stress-inducible. The OsAKR1 recombinant protein exhibited a high nicotinamide adenine dinucleotide phosphate-dependent catalytic activity to reduce toxic aldehydes including glycolysis-derived methylglyoxal (MG) and lipid peroxidation-originated malondialdehyde (MDA). The function of this enzyme in MG detoxification was demonstrated in vivo in E. coli and in transgenic plants overproducing the OsAKR1 protein. Heterologous synthesis of the OsAKR1 enzyme in transgenic tobacco plants resulted in increased tolerance against oxidative stress generated by methylviologen (MV) and improved resistance to high temperature. In these plants lower levels of MDA were detected both following MV and heat treatment due to the activity of the OsAKR1 enzyme. The transgenic tobaccos also exhibited higher AKR activity and accumulated less MG in their leaves than the wild type plants; both in the presence and absence of heat stress. These results support the positive role of OsAKR1 in abiotic stress-related reactive aldehyde detoxification pathways and its use for improvement of stress tolerance in plants.
Journal Article•
TL;DR: Evidence of oxidative stress, mitochondrial dysfunction and impaired calcium extrusion in GLC cells compared to NLC cells is found and suggests their importance in the pathological changes occurring at the ONH in glaucoma.
Abstract: Purpose: Oxidative stress is implicit in the pathological changes associated with glaucoma The purpose of this study was to compare levels of oxidative stress in glial fibrillary acid-negative protein (GFAP) lamina cribrosa (LC) cells obtained from the optic nerve head (ONH) region of 5 normal (NLC) and 4 glaucomatous (GLC) human donor eyes and to also examine mitochondrial function and calcium homeostasis in this region of the ONH Methods: Intracellular reactive oxygen species (ROS) production was examined by a thiobarbituric acid reactive substances (TBARS) assay which measures malondialdehyde (MDA), a naturally occurring product of lipid peroxidation and is used as an indicator of oxidative stress Mitochondrial membrane potential (MMP) and intracellular calcium ([Ca2+]i) levels were evaluated by flow cytometry using the JC-1 (5,5′,6,6′-tetrachloro-1,1′,3,3′tetrabenzimidazolecarbocyanine iodide) and fluo-4/AM probes respectively Anti-oxidant and Ca 2+ transport system gene and protein expression were determined by real time polymerase chain reaction (RT-PCR) using gene-specific primer/ probe sets and western immunoblotting, respectively Results: Intracellular ROS production was increased in GLC compared to NLC (2719±705 µM MDA versus 1459±082 µM MDA, p<005) Expression of the anti-oxidants Aldo-keto reductase family 1 member C1 (AKR1C1) and Glutamate cysteine ligase catalytic subunit (GCLC) were significantly lower in GLC (p=002) compared to NLC control MMP was lower in GLC (575±68%) compared to NLC (418±53%) [Ca 2+ ]i levels were found to be higher (p<0001) in GLC cells compared to NLC Expression of the plasma membrane Ca2+/ATPase (PMCA) and the sodium-calcium (NCX) exchangers were lower, while intracellular sarco-endoplasmic reticulum Ca2+/ATPase 3 (SERCA) expression was significantly higher in GLC compared to NLC Subjection of NLC cells to oxidative stress (200 µM H202) reduced expression of Na+/Ca2+ exchanger 1 (NCX 1), plasma membrane Ca2+ ATPase 1 (PMCA 1), and PMCA 4 as determined by RT–PCR Conclusions: Our data finds evidence of oxidative stress, mitochondrial dysfunction and impaired calcium extrusion in GLC cells compared to NLC cells and suggests their importance in the pathological changes occurring at the ONH in glaucoma Future therapies may target reducing oxidative stress and / or [Ca2+]i
TL;DR: Ginger exhibit a neuroprotective effect by accelerating brain anti-oxidant defense mechanisms and down regulating the MDA levels to the normal levels in the diabetic rats, suggesting that ginger may be used as therapeutic agent in preventing complications in diabetic patients.
TL;DR: It was revealed that supplemental ASX for 3 weeks improved oxidative stress biomarkers by suppressing lipid peroxidation and stimulating the activity of the antioxidant defense system.
Abstract: Oxidative stress is caused by an imbalance between the antioxidant and the reactive oxygen species, which results in damage to cells or tissues Recent studies have reported that oxidative stress is involved in obesity, in addition to many other human diseases and aging A prospective, randomized, double-blind study was performed to investigate the effect of astaxanthin (ASX), which is known to be a potent antioxidant, on oxidative stress in overweight and obese adults in Korea Twenty-three adults with BMI > 250 kg/m2 enrolled in this study and were randomly assigned to two dose groups: ASX 5 mg and 20 mg once daily for 3 weeks Malondialdehyde (MDA), isoprostane (ISP), superoxide dismutase (SOD) and total antioxidant capacity (TAC), as oxidative stress biomarkers, were measured at baseline and 1, 2 and 3 weeks after ASX administration Compared with baseline, the MDA (by 346% and 352%) and ISP (by 649% and 647%) levels were significantly lowered, whereas SOD (by 193% and 194%) and TAC (by 121% and 125%) levels were significantly increased in two dose groups after the 3 week intervention This study revealed that supplemental ASX for 3 weeks improved oxidative stress biomarkers by suppressing lipid peroxidation and stimulating the activity of the antioxidant defense system Copyright © 2011 John Wiley & Sons, Ltd
01 Jan 2011
TL;DR: Increased oxidative stress and decreased antioxidants as one of the important contributing factor in the pathogenesis of primary dysmenorrhea is revealed.
Abstract: Objectives: Primary dysmenorrhea is the menstrual pain asso ciated with ovulatory cycles in the absence of pathological findings common in adolescents. Oxygen free radicals and the formation of primary dysmenorrhea is closely related to atrial contraction of uterine smooth muscle. The present study was to investigate the oxidative stress and antioxidants status in primary dysmenorrhea. Methods: A 45 cases of primary dysmenorrhea and 25 age and sex matched controls were included in the study. The lipid peroxidation status was measured by estimating malondialdehyde. The anti oxidant status was measured by estimating reduced glutathione, superoxide dismutase, vitamin E and vitamin C respectively. Reslults: The malondialdehyde level was increased in cases than controls (p = 0.001). The antioxidant parameters studied like reduced glutathione, superoxide dismutase, vitamin E and vitamin C, all were decreased individually in cases than controls respectively (p = 0.001). Conclusions: Our study showed a significant increased lipid per oxidation and decreased anti oxidants levels in primary dysmenorrhea cases than controls. This study reveals increased oxidative stress and decreased antioxidants as one of the important contributing factor in the pathogenesis of primary dysmenorrhea.
TL;DR: The results indicate that changes in redox status occur during reproduction in house mice, but suggest that females use mechanisms to cope with the consequences of increased energetic demands and limit oxidative stress.
Abstract: Investment in reproduction is costly and frequently decreases survival or future reproductive success. However, the proximate underlying causes for this are largely unknown. Oxidative stress has been suggested as a cost of reproduction and several studies have demonstrated changes in antioxidants with reproductive investment. Here, we test whether oxidative stress is a consequence of reproduction in female house mice (Mus musculus domesticus), which have extremely high energetic demands during reproduction, particularly through lactation. Assessing oxidative damage after a long period of reproductive investment, there was no evidence of increased oxidative stress, even when females were required to defend their breeding territory. Instead, in the liver, markers of oxidative damage (malonaldehyde, protein thiols and the proportion of glutathione in the oxidized form) indicated lower oxidative stress in reproducing females when compared with non-reproductive controls. Even during peak lactation, none of the markers of oxidative damage indicated higher oxidative stress than among non-reproductive females, although a positive correlation between protein oxidation and litter mass suggested that oxidative stress may increase with fecundity. Our results indicate that changes in redox status occur during reproduction in house mice, but suggest that females use mechanisms to cope with the consequences of increased energetic demands and limit oxidative stress.
TL;DR: In this paper, the authors demonstrated that exogenous hydrogen peroxide (H2O2) was able to improve the tolerance of wheat seedlings to salt stress by decreasing the concentration of malondialdehyde (MDA), increasing the activity of superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), and ascorbate peroxidation (APX).
Abstract: Hydrogen peroxide (H2O2), an active oxygen species, is widely generated in many biological systems and mediates various physiological and biochemical processes in plants. In this study, we demonstrated that exogenous H2O2 was able to improve the tolerance of wheat seedlings to salt stress. Treatments with exogenous H2O2 for 2 days significantly enhanced salt stress tolerance in wheat seedlings by decreasing the concentration of malondialdehyde (MDA), the production rate of superoxide radical (O2
−), and increasing the activities of superoxide dismutase (SOD), peroxidase (POD), catalase (CAT) and ascorbate peroxidase (APX), and the concentration of glutathione (GSH) and carotenoids (CAR). To further clarify the role of H2O2 in preventing salt stress damage, CAT and ascorbate (AsA), the specific H2O2 scavengers, were used. The promoting effect of exogenous H2O2 on salt stress could be reversed by the addition of CAT and AsA. It was suggested that exogenous H2O2 induced changes in MDA, O2
−, antioxidant enzymes and antioxidant compounds were responsible for the increase in salt stress tolerance observed in the experiments. Therefore, H2O2 may participate in antioxidant enzymes and antioxidant compounds induced tolerance of wheat seedlings to salt stress. The results also showed that exogenous H2O2 had a positive physiological effect on the growth and development of salt-stressed seedlings.
TL;DR: It is concluded that acute low temperature can induce oxidative stress, DNA damage, lipid peroxidation and changes in osmolality in L. vannamei.
Abstract: To evaluate the genotoxic, physiological and immunological effects of short-term acute low temperature stress on the Pacific white shrimp, Litopenaeus vannamei, we rapidly transferred shrimp from tanks at 23±2 °C to aquaria at the same temperature (controls) or 12±2 °C for 12 h. Changes in the shrimp hemocyte respiratory burst activity and DNA damage were examined during and after exposure to the temperature stress using flow cytometry and the comet assay, respectively. We also monitored changes in the total hemocyte count, malondialdehyde levels, total protein concentration and osmolality in shrimp plasma. The results show that hemocyte respiratory burst activity, malondialdehydes levels and hemocyte DNA damage in the plasma all increased significantly after exposure to 12±2 °C for 3 h. In contrast, total hemocyte count, total protein concentration and osmolality in the plasma decreased compared to the controls. We conclude that acute low temperature can induce oxidative stress, DNA damage, lipid peroxidation and changes in osmolality in L. vannamei.
TL;DR: Results indicate the involvement of oxidative stress and apoptosis in A549 cells exposed to MWCNTs and provide insights of the mechanisms involved in M WCNTs-induced apoptosis at cellular level.
Abstract: Multi-walled carbon-nanotubes (MWCNTs)-induced apoptotic changes were studied in human lung epithelium cell line-A549. Non-cytotoxic doses of MWCNTs were identified using tetrazolium bromide salt (MTT) and lactate dehydrogenase (LDH) release assays. Cells were exposed to MWCNTs (0.5-100 μg/ml) for 6-72 h. Internalization and characterization of CNTs was performed by electron microscopy. Apoptotic changes were estimated by nuclear condensation, DNA laddering, and confirmed by expression of associated markers: p(53), p(21WAF1/CIP1), Bax, Bcl(2) and activated caspase-3. MWCNTs induced the production of reactive oxygen species and malondialdehyde along with significant decrease in the activity of catalase and glutathione. MWCNTs-induced ROS generation was found not to be associated with the mitochondrial activity. In general, the changes were significant at 10 and 50 μg/ml only. Results indicate the involvement of oxidative stress and apoptosis in A549 cells exposed to MWCNTs. Our studies provide insights of the mechanisms involved in MWCNTs-induced apoptosis at cellular level.
TL;DR: It is demonstrated that ginsenoside Rd exerts neuroprotection in transient focal ischemia, which may involve early free radicals scavenging pathway and a late anti-inflammatory effect.
TL;DR: Salivary MDA levels, a product of lipid peroxidation, were significantly increased among diabetics together with uric acid and reduced glutathione levels were similar to those of the control group.
Abstract: Background: The aim of this study was to assess the salivary content of lipid peroxidation and antioxidants in patients with type 2 diabetes.Method: We studied 25 patients with type 2 diabetes and ...
TL;DR: It is shown that activation of β‐receptors increases the production of reactive oxygen species (ROS) in the heart cell, which generates enhanced Ca2+ fluxes and more vigorous contraction and might contribute to the understanding of diseases with defective cardiac contraction, such as heart failure.
Abstract: The sympathetic adrenergic system plays a central role in stress signalling and stress is often associated with increased production of reactive oxygen species (ROS). Furthermore, the sympathetic adrenergic system is intimately involved in the regulation of cardiomyocyte Ca2+ handling and contractility. In this study we hypothesize that endogenously produced ROS contribute to the inotropic mechanism of β-adrenergic stimulation in mouse cardiomyocytes. Cytoplasmic Ca2+ transients, cell shortening and ROS production were measured in freshly isolated cardiomyocytes using confocal microscopy and fluorescent indicators. As a marker of oxidative stress, malondialdehyde (MDA) modification of proteins was detected with Western blotting. Isoproterenol (ISO), a β-adrenergic agonist, increased mitochondrial ROS production in cardiomyocytes in a concentration- and cAMP–protein kinase A-dependent but Ca2+-independent manner. Hearts perfused with ISO showed a twofold increase in MDA protein adducts relative to control. ISO increased Ca2+ transient amplitude, contraction and L-type Ca2+ current densities (measured with whole-cell patch-clamp) in cardiomyocytes and these increases were diminished by application of the general antioxidant N-acetylcysteine (NAC) or the mitochondria-targeted antioxidant SS31. In conclusion, increased mitochondrial ROS production plays an integral role in the acute inotropic response of cardiomyocytes to β-adrenergic stimulation. On the other hand, chronically sustained adrenergic stress is associated with the development of heart failure and cardiac arrhythmias and prolonged increases in ROS may contribute to these defects.