Guanidinoacetate Inhibits Glutamate Uptake in Rat Striatum of Rats at Different Ages

Glutamate plays a central role in the excitatory synaptic transmission and is important for brain development and functioning. Increased glutamate levels in the synaptic cleft are related to neuronal damage associated with excitotoxicity. Guanidinoacetate methyltransferase (GAMT) deficiency is an inherited neurometabolic disorder biochemically characterized by tissue accumulation of guanidinoacetate (GAA) and depletion of creatine. Affected patients present epilepsy and mental retardation whose pathogeny is unclear. In the present study we investigated the in vitro and in vivo (intrastriatal administration) effect of GAA on glutamate uptake by striatum slices of developing and adult rats. Results showed that GAA significantly inhibited in vitro glutamate uptake at 50 μM and 100 μM in all ages tested. We also tested the effect of taurine on the inhibition of glutamate uptake caused by GAA. Taurine significantly attenuated the inhibitory effect caused by 50 μM GAA, but did not alter that provoked by 100 μM GAA. Furthermore, intrastriatal administration of a solution of 30 μM GAA (0.06 nmol/striatum) significantly inhibited glutamate uptake by rat striatum slices. Our results suggest that the inhibition of striatal glutamate uptake caused by GAA might be involved in the neuropathology and especially in the acute neurological features present in patients with GAMT-deficiency.     

Control of Redox Balance by the Stringent Response Regulatory Protein Promotes Antioxidant Defenses of Salmonella

We report herein a critical role for the stringent response regulatory DnaK suppressor protein (DksA) in the coordination of antioxidant defenses. DksA helps fine-tune the expression of glutathione biosynthetic genes and discrete steps in the pentose phosphate pathway and tricarboxylic acid cycle that are associated with the generation of reducing power. Control of NAD(P)H/NAD(P)⁺ redox balance by DksA fuels downstream antioxidant enzymatic systems in nutritionally starving Salmonella. Conditional expression of the glucose-6-phosphate dehydrogenase-encoding gene zwf, shown here to be under DksA control, increases both the NADPH pool and antioxidant defenses of dksA mutant Salmonella. The DksA-mediated coordination of redox balance boosts the antioxidant defenses of stationary phase bacteria. Not only does DksA increase resistance of Salmonella against hydrogen peroxide (H₂O₂), but it also promotes fitness of this intracellular pathogen when exposed to oxyradicals produced by the NADPH phagocyte oxidase in an acute model of infection. Given the role of DksA in the adjustment of gene expression in most bacteria undergoing nutritional deprivation, our findings raise the possibility that the control of central metabolic pathways by this regulatory protein maintains redox homeostasis essential for antioxidant defenses in phylogenetically diverse bacterial species.     

Experimental Evidence that Methylmalonic Acid Provokes Oxidative Damage and Compromises Antioxidant Defenses in Nerve Terminal and Striatum of Young Rats

Methylmalonic acidemia and propionic acidemia are organic acidemias biochemically characterized by predominant tissue accumulation of methylmalonic acid (MMA) and propionic acid (PA), respectively. Affected patients present predominantly neurological symptoms, whose pathogenesis is not yet fully established. In the present study we investigated the in vitro effects of MMA and PA on important parameters of lipid and protein oxidative damage and on the production of reactive species in synaptosomes from cerebrum of developing rats. Synaptosomes correspond to nerve terminals that have been used to investigate toxic properties of compounds on neuronal cells. The in vivo effects of intrastriatal injection of MMA and PA on the same parameters and on enzymatic antioxidant defenses, were also studied. MMA-induced in vitro and in vivo lipid peroxidation and protein oxidative damage. Furthermore, the lipid oxidative damage was attenuated or prevented, pending on the doses utilized, by the free radical scavengers α-tocopherol, melatonin and by the NMDA glutamate receptor antagonist MK-801, implying the involvement of reactive species and glutamate receptor activation in these effects. In addition, 2′,7′-dichlorofluorescein diacetate oxidation was significantly increased in synaptosomes by MMA, reinforcing that reactive species generation is elicited by this organic acid. We also verified that glutathione peroxidase activity was inhibited by intrastriatal MMA injection. In contrast, PA did not induce any significant effect on all parameters examined in vitro and in vivo, implying a selective action for MMA. The present data demonstrate that oxidative stress is induced by MMA in vitro in nerve terminals and in vivo in striatum, suggesting the participation of neuronal cells in MMA-elicited oxidative damage.     

蛋白激酶组在玉米叶片ABA和H202诱导抗氧化防护中的作用

蛋白磷酸化在植物细胞脱落酸（ABA）介导的信号转导中起重要作用。然而,很多参与ABA信号途径的蛋白元件仍不清楚。使用改进的体外激酶试验方法的研究结果表明,在玉米叶片中,ABA和H2O2能够快速活化蛋白激酶总活性和ca^2＋依赖型蛋白激酶总活性;ABA诱导的蛋白激酶总活性增加可以被活性氧的抑制剂和清除剂抑制,蛋白激酶抑制剂不仅可以降低ABA和H2O2诱导的激酶活性增加,而且也可以弱化它们对抗氧化防护酶活性的诱导作用;ABA和H2O2引发的蛋白磷酸化作用显著居先于它们诱导的抗氧化防护作用。使用凝胶激酶试验方法进行研究发现,一组分子量分别为66kDa,52kDa,49kDa和35kDa的蛋白激酶可能介导了ABA和H2O2诱导的抗氧化防护反应,并且66kDa和49kDa的蛋白激酶可能在ROS的下游起作用,而52kDa和35kDa的蛋白激酶可能在ABA和ROS的下游起作用。     

Role of Protein Kinases in Abscisic Acid and H2O2 Induced Antioxidant Defense in Maize

Protein phosphorylation plays a central role in mediating abscisic acid (ABA) signaling transduction in plant cells, whereas many of the sensory proteins involving in ABA signaling pathway remain unclear. Here, using a modified in vitro kinase assay, our results showed that ABA and H2O2 induced a rapid activation of total protein kinases and calcium dependent protein kinases in the leaves of maize seedlings. However, ABA-induced activation of protein kinases was inhibited by reactive oxygen species (ROS) inhibitors or scavengers. Protein kinase inhibitors decelerated not only the ABA and H2O2 -induced kinase activity but also ABA or H2O2-induced antioxidant enzyme activity. Protein phosphorylation caused by ABA and H2O2 preceded ABA or H2O2 -induced antioxidant defense obviously. Using in-gel kinase assays, our results showed that several protein kinases with molecular masses of 66kDa, 52kDa, 49kDa and 35kDa respectively might mediate ABA and H2O2-induced antioxidant defense. And the 66kDa and 49kDa protein kinases may act downstream of ROS, and the 52kDa and 35kDa protein kinases may act between ABA and ROS in ABA-induced antioxidant defensive signaling.     

蛋白激酶组在玉米叶片ABA和H_2O_2诱导抗氧化防护中的作用(英文)

蛋白磷酸化在植物细胞脱落酸(ABA)介导的信号转导中起重要作用。然而,很多参与ABA信号途径的蛋白元件仍不清楚。使用改进的体外激酶试验方法的研究结果表明,在玉米叶片中,ABA和H2O2能够快速活化蛋白激酶总活性和Ca2+依赖型蛋白激酶总活性;ABA诱导的蛋白激酶总活性增加可以被活性氧的抑制剂和清除剂抑制,蛋白激酶抑制剂不仅可以降低ABA和H2O2诱导的激酶活性增加,而且也可以弱化它们对抗氧化防护酶活性的诱导作用;ABA和H2O2引发的蛋白磷酸化作用显著居先于它们诱导的抗氧化防护作用。使用凝胶激酶试验方法进行研究发现,一组分子量分别为66kDa,52kDa,49kDa和35kDa的蛋白激酶可能介导了ABA和H2O2诱导的抗氧化防护反应,并且66kDa和49kDa的蛋白激酶可能在ROS的下游起作用,而52kDa和35kDa的蛋白激酶可能在ABA和ROS的下游起作用。     

Activation of Endogenous Antioxidant Defenses in Neuronal Cells Prevents Free Radical-Mediated Damage

Abstract: Dopamine (DA) is oxidized to the neurotoxic prooxidant species H₂O₂, OH^•, and DA quinones. We tested whether dimethyl fumarate (DMF), an electrophile shown to induce a pleiotropic antioxidant response in nonneuronal cells, could reduce the toxicity of DA metabolites in neural cells. Treatment of the N18-RE-105 neuroblastoma-retina hybridoma cell line with 30–150 µ M dopamine led to cell death within 24 h, which increased steeply with dose, decreased with higher plating density, and was blocked by the H₂O₂-metabolizing enzyme catalase. Pretreatment with DMF (30 µ M , 24 h) significantly attenuated DA and H₂O₂ toxicity (40–60%) but not that caused by the calcium ionophore ionomycin. DMF treatment also elevated total intracellular GSH and increased activities of the antioxidant enzymes quinone reductase (QR), glutathione S -transferase (GST), glutathione reductase, and the pentose phosphate enzyme glucose-6-phosphate dehydrogenase. To assess the protective efficacy of QR and GST, a stable cell line was constructed in which these enzymes were overexpressed. Cell death in the overexpressing line was not significantly different from that in a cell line expressing normal QR and GST activities, indicating that these two enzymes alone are insufficient for protection against DA toxicity. Although the relative importance of a single antioxidant enzyme such as QR or GST may be small, antioxidant inducers such as DMF may prove valuable as agents that elicit a broad-spectrum neuroprotective response.     

蛋白激酶组在玉米叶片ABA和H2O2诱导抗氧化防护中的作用

蛋白磷酸化在植物细胞脱落酸（ABA）介导的信号转导中起重要作用。然而,很多参与ABA信号途径的蛋白元件仍不清楚。使用改进的体外激酶试验方法的研究结果表明,在玉米叶片中,ABA和H2O2能够快速活化蛋白激酶总活性和Ca2+依赖型蛋白激酶总活性;ABA诱导的蛋白激酶总活性增加可以被活性氧的抑制剂和清除剂抑制,蛋白激酶抑制剂不仅可以降低ABA和H2O2诱导的激酶活性增加,而且也可以弱化它们对抗氧化防护酶活性的诱导作用;ABA和H2O2引发的蛋白磷酸化作用显著居先于它们诱导的抗氧化防护作用。使用凝胶激酶试验方法进行研究发现,一组分子量分别为66kDa, 52kDa, 49kDa和35kDa的蛋白激酶可能介导了ABA和H2O2诱导的抗氧化防护反应,并且66kDa和49kDa的蛋白激酶可能在ROS的下游起作用, 而52kDa和35kDa的蛋白激酶可能在ABA和ROS的下游起作用。     

锌胁迫对桉树巯基物质含量及抗氧化酶活性的影响

通过桉树的水培实验,测定了不同浓度Zn胁迫下桉树的生物量,根和叶中Zn、巯基物质(非蛋白巯基,谷胱甘肽和植物络合素)和丙二醛(MDA)的含量,以及根中抗氧化酶的活性。从巯基物质含量和抗氧化酶活性的角度,探讨了桉树抵御Zn胁迫造成氧化性伤害的机制。实验结果表明,Zn浓度较低(20 mg/L和40 mg/L)时,根中MDA含量非显著性增加,抗氧化酶超氧化物歧化酶(SOD)、过氧化物酶(POD)和过氧化氢酶(CAT)的活性上升,叶中巯基物质含量非显著性增加。Zn浓度较高(120 mg/L和140 mg/L)时,根中MDA含量显著性增加,SOD、POD和CAT的活性下降,叶中巯基物质含量显著性增加。因此,低浓度Zn胁迫时,桉树中巯基物质和抗氧化酶系统对氧化性伤害有较好的缓解作用;高浓度Zn胁迫时,大量过氧化物积累,桉树中巯基物质和抗氧化酶系统对氧化损伤的缓解作用降低。     

菹草提取物总黄酮、总酚酸和抗氧化活性含量研究

研究菹草提取物的有效成分,测定其总黄酮含量及总酚酸含量,并确定它的乙酸乙酯和石油醚部位的抗氧化活性成分。采用紫外可见分光光度法,以芦丁和没食子酸作为控制材料,测定菹草的石油醚部位及乙酸乙酯部位中总黄酮和总酚酸含量;采用清除DPPH自由基能力测定法、测定总还原能力铁氰化钾法和水杨酸捕捉羟基自由基法来对菹草各组分提取物的抗氧化能力进行研究。菹草中有一定量的黄酮类化合物和酚酸类化合物存在,不同溶剂提取的部位所含有的总黄酮和总酚酸含量是有差异的,石油醚部位的总黄酮含量要高于乙酸乙酯部位的总黄酮含量,并且总酚酸的含量亦是如此;石油醚部位和乙酸乙酯部位的提取物具有清除DPPH、羟基自由基和还原Fe^3+的能力,各部位清除DPPH、羟基自由基的能力和还原Fe^3+的能力随着样品浓度的增大而增大,且乙酸乙酯部位的测定结果均低于石油醚部位。     

冬眠哺乳动物氧化应激产生及抗氧化防御机制研究进展

哺乳动物的冬眠是一种季节性异温状态,是对外界恶劣自然环境的一种适应策略。冬眠-阵间觉醒周期中,伴随着生理功能的剧烈变化,从冬眠期间整体代谢的抑制,到阵间觉醒时氧代谢的急剧增加,使动物体内产生了大量的氧自由基。然而,冬眠动物出眠时并未表现出明显的氧化损伤迹象,因此,冬眠哺乳动物被认为是一种天然的抗氧化损伤模型。本文从氧化应激的产生、活性氧的来源、抗氧化防御等方面综述了冬眠哺乳动物对氧化应激的防御,并从其抗氧化的分子调控方面分析了冬眠哺乳动物对氧化应激的适应机制。     

动物抗氧化系统中主要抗氧化酶基因的研究进展

抗氧化系统是机体清除体内多余的活性氧、保护自身免受氧化损伤的重要体系,其中超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶等起主要作用。本文将对动物抗氧化系统中,超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶基因的种类、分布、结构及表达进行综述。     

Antioxidant defense and trace element imbalance in patients with postradiation syndrome

More than 6000 residents of Latvia were involved in recovery work in Chernobyl. They were healthy men exposed to substantial ionizing radiation (0.01–0.5 Gy). Now, these recovery workers suffer from “postradiation syndrome”: dizziness and poor memory, headache, local pains, and so forth. The biochemical mechanism of “postradiation syndrome” has not been completely established. In this Phase I study, we have investigated how exposure to radiation impacts antioxidative defense and trace element concentrations in the blood of recovery workers. Thirty-five patients with postradiation syndrome (men, age range 33–50 yr) and 15 healthy men similar in age as control subjects were studied for the effects on plasma chemiluminescence, the activity of antioxidant enzymes, and the concentration of ceruloplasmin and concentrations of selenium (Se), zinc (Zn), and copper (Cu) in blood. The results revealed that plasma chemiluminescence was significantly increased (3.5-fold to 5.5-fold), the activity of catalase in erythrocytes was significantly elevated, and the activity of glutathione peroxidase in plasma was significantly reduced in examined patients. Concentrations of Zn and Cu were significantly higher and the concentration of Se was lower in these patients. We conclude that the patients exposed to ionizing radiation have diminished blood antioxidant defense associated with pronounced Se deficiency and imbalance of Zn and Cu. Presented in part on the SFRR (Europe) Summer Meeting in Dresden, July 2–5, 1999.     

Glycine Provokes Lipid Oxidative Damage and Reduces the Antioxidant Defenses in Brain Cortex of Young Rats

Patients affected by nonketotic hyperglycinemia (NKH) usually present severe neurological symptoms and suffer from acute episodes of intractable seizures with leukoencephalopathy. Although excitotoxicity seems to be involved in the brain damage of NKH, the mechanisms underlying the neuropathology of this disease are not fully established. The objective of the present study was to investigate the in vitro effects of glycine (GLY), that accumulate at high concentrations in the brain of patients affected by this disorder, on important parameters of oxidative stress, such as lipid peroxidation (thiobarbituric acid-reactive substances (TBA-RS) and chemiluminescence) and the most important non-enzymatic antioxidant defense reduced glutathione (GSH) in cerebral cortex from 30-day-old rats. GLY significantly increased TBA-RS and chemiluminescence values, indicating that this metabolite provokes lipid oxidative damage. Furthermore, the addition of high doses of the antioxidants melatonin, trolox (soluble vitamin E) and GSH fully prevented GLY-induced increase of lipid peroxidation, indicating that free radicals were involved in this effect. GLY also decreased GSH brain concentrations, which was totally blocked by melatonin treatment. Finally, GLY significantly reduced sulfhydryl group content from a commercial GSH solution, but did not oxidize reduced cytochrome C. Our data indicate that oxidative stress elicited in vitro by GLY may possibly contribute at least in part to the pathophysiology of the neurological dysfunction in NKH.     

Liver Nonprotein Sulfhydryl and Taurine Concentrations,and Fat Content of Rats Fed a Low Protein Diet Supplemented with Sulfur-containing Amino Acids

The relative excess of some catabolites of sulfur-containing amino acids in the liver of rats fed a low protein diet might be one of the factors which cause the liver fat accumulation. To investigate the possibility were studied relationships between changes in concentrations of some metabolites of sulfur-containing amino acids and those in fat contents of rats fed a low protein diet consisting of heated soybean flour, casein or wheat flour with or without added methionine, threonine or lysine. The addition of 0.6% methionine to the 25% heated soybean flour diet increased the nonprotein-sulfhydryl (NP–SH) concentration and fat content in the liver. These changes were prevented by the further addition of 0.5% threonine to the diet, although the NP–SH concentration was remarkably higher than that of rats fed the unsupplemented diet. The addition of 0.6% cystine HC1 to the 25% heated soybean flour diet containing sufficient choline elevated the NP–SH concentration and fat content in the liver, which were not affected by the further addition of 0.5% threonine. The addition of 0.6% cystine HC1 to the 10% casein diet significantly increased the fat content, and NP–SH and taurine concentrations in the liver. The further addition of 0.5 % threonine completely decreased the fat content, and partially reduced the NP–SH and taurine concentrations. Effects of supplementation of 0.4% lysine HC1 to the 70% wheat flour diet on the fat content and NP–SH concentration in the liver demonstrated the trends similar to those of supplementation of cystine to the 10% casein diet. The further addition of threonine remarkably decreased the fat content, NP–SH and taurine concentrations in the liver.     

Benfotiamine Enhances Antioxidant Defenses and Protects against Cisplatin‐Induced DNA Damage in Nephrotoxic Rats

The objective of the present study was to assess superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), paraoxonase (PON1), glutathione reductase (GR), and catalase (CAT) activities ratio and their relationship with DNA oxidative damage in rats treated with cisplatin (3 mg/kg bwt/day) in the presence and absence of benfotiamine (100 mg/kg/day) for 25 days. Cisplatin‐induced renal damage was evidenced by renal dysfunction and elevated oxidative stress markers. SOD activity and levels of nitric oxide, protein carbonyl, malondialdehyde, and 8‐hydroxy‐2'‐deoxyguanosine were significantly increased by cisplatin treatment. Moreover, the ratios of GPx/GR, SOD/GPx, SOD/CAT, and SOD/PON1 were significantly increased compared to control. In contrast, glutathione levels were significantly decreased by cisplatin treatment. Simultaneous treatment of rats with cisplatin and benfotiamine ameliorate these variables to values near to those of control rats. This study suggests that benfotiamine can prevent cisplatin‐induced nephrotoxicity by inhibiting formation reactive species of oxygen and nitrogen. © 2013 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:398‐405, 2013; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.21501     

急性低温对黑鲷抗氧化酶活性和 热休克蛋白含量的影响

为探究急性低温胁迫对黑鲷（Acanthopagrus schlegelii）生理机能的影响,以1龄黑鲷作为实验鱼,以15 ℃为对照组,设置10 ℃和5 ℃作为低温胁迫组,处理24 h后再转入15 ℃的水体中进行恢复实验,测定不同温度、不同时间点下1龄黑鲷肝的抗氧化酶活性以及热休克蛋白（Hsp）含量的变化。研究结果显示,低温胁迫实验中,低温处理组（10 ℃和5 ℃）在急性低温胁迫的24 h内,超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-PX）活性和热休克蛋白含量均呈现先上升后下降的趋势。10 ℃处理组上述三种抗氧化酶活性皆在12 h达到最大值,超氧化物歧化酶、过氧化氢酶活性24 h恢复到对照水平,而谷胱甘肽过氧化物酶在18 h已经恢复到正常水平;在5 ℃处理组,超氧化物歧化酶和过氧化氢酶活性在6 h达到最大值,谷胱甘肽过氧化物酶在18 h达到最大值,且在24 h都仍与对照组有极显著差异,超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶活性分别在恢复实验的12 h、12 h和6 h恢复到对照组水平。10 ℃和5 ℃两个处理组的热休克蛋白含量皆在胁迫18 h达到最大,10 ℃处理组在24 h恢复到正常水平,但5 ℃处理组的热休克蛋白含量直到恢复实验结束仍与对照组存在差异。本实验结果表明,急性低温胁迫对超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和热休克蛋白具有显著影响,其均呈现有规律的变化趋势,说明上述酶和蛋白参与了黑鲷的低温胁迫应答过程,通过协同调节黑鲷的生理机能使其适应环境变化,减少急性低温对鱼体的损伤并使其能够在环境骤变情况下存活下来。只有在自我调节范围内,黑鲷随着胁迫时间的延长,其体内才能够建立新的生理平衡来适应低温,因此在黑鲷养殖过程中,应当注意水温不宜低于5 ℃,水温过低时,应尽快将其移入室内,避免水温骤降对鱼体造成损伤。     

Antioxidant and intestinal anti-inflammatory effects of plant-derived coumarin derivatives

BackgroundCoumarins, also known as benzopyrones, are plant-derived products with several pharmacological properties, including antioxidant and anti-inflammatory activities. Based on the wide distribution of coumarin derivatives in plant-based foods and beverages in the human diet, our objective was to evaluate both the antioxidant and intestinal anti-inflammatory activities of six coumarin derivatives of plant origin (scopoletin, scoparone, fraxetin, 4-methyl-umbeliferone, esculin and daphnetin) to verify if potential intestinal anti-inflammatory activity was related to antioxidant properties.MethodsIntestinal inflammation was induced by intracolonic instillation of TNBS in rats. The animals were treated with coumarins by oral route. The animals were killed 48 h after colitis induction. The colonic segments were obtained after laparotomy and macroscopic and biochemical parameters (determination of glutathione level and myeloperoxidase and alkaline phosphatase activities) were evaluated. The antioxidant properties of these coumarins were examined by lipid peroxidation and DPPH assays.ResultsTreatment with esculin, scoparone and daphnetin produced the best protective effects. All coumarin derivatives showed antioxidant activity in the DPPH assay, while daphnetin and fraxetin also showed antioxidant activity by inhibiting lipid peroxidation. Coumarins, except 4-methyl-umbeliferone, also showed antioxidant activity through the counteraction of glutathione levels or through the inhibition of myeloperoxidase activity.DiscussionThe intestinal anti-inflammatory activity of coumarin derivatives were related to their antioxidant properties, suggesting that consumption of coumarins and/or foods rich in coumarin derivatives, particularly daphnetin, esculin and scoparone, could prevent intestinal inflammatory disease.     

蓝莓果渣提取物总酚含量及抗氧化活性研究

研究了蓝莓果渣提取物总酚含量及其抗氧化活性。分别采用水、40%乙醇及纤维素酶辅助乙醇超声提取蓝莓果渣,并用Folin-Ciocalteu试剂对3种提取物的总酚含量进行评估;并采用DPPH清除实验及O2—.清除实验对3种提取物的抗氧化活性进行研究。实验结果表明,纤维素酶辅助超声提取蓝莓果渣的总酚含量最高,可达425.36±15.21 mg GAE.100 g-1DW,远远高于水提物(169.46±9.75 mg GAE.100 g-1DW)及醇提物(218.39±12.54mg GAE.100 g-1DW)中的总酚含量。且纤维素酶辅助乙醇超声提取物对DPPH的清除能力为2.67±0.13 gVc.100 g-1DW,对O—.2的清除能力2.48±0.14 g Vc.100 g-1DW,明显好于醇提物及水提物抗氧化活性。     

Antioxidant Defenses in Fish: Biotic and Abiotic Factors

Oxygen in its molecular state O₂, is essential for many metabolic processes that are vital to aerobic life. Aerobic organisms cannot exist without oxygen, which nevertheless is inherently dangerous to their lives. Like all aerobic organisms, fish are also susceptible to the effects of reactive oxygen and have inherent and effective antioxidant defenses that are well described in the literature. This review investigates the influence of different biotic and abiotic factors (age, phylogenetic position, feeding behavior, environmental factors, oxygen, temperature, presence of xenobiotics) on antioxidant defenses in fish. Studies of antioxidant activity in fish open a number of novel research lines providing greater knowledge of fish physiology, which will benefit various aspects of fish farming and artificial production.