海洋微藻响应重金属复合胁迫的生理生态学机制

重金属污染物进入海洋环境会破坏海洋生态系统的结构和功能。海洋微藻构成了海洋食物链的基础, 是海洋生态系统主要的初级生产者。重金属复合胁迫对海洋微藻产生毒性效应, 会阻碍藻细胞分裂、破坏DNA结构、抑制光合作用、减少细胞色素合成、导致藻细胞畸变以及改变浮游植物种类组成等。海洋微藻在长期种系进化或个体发育过程中, 形成了一系列响应重金属复合胁迫的特殊生理生态机制。它们可以利用由酶类和非酶类组成的抗逆保护系统, 减轻重金属复合胁迫导致的生物毒害作用; 还可以通过调节金属硫蛋白(Metallothionein, MT)等相关蛋白基因表达以维持正常的生理功能。探究海洋微藻响应重金属复合胁迫的生理生态学机制, 有利于为海洋重金属污染的生物修复提供依据, 具有重要的理论与现实意义。     

重金属镉和铅胁迫对海洋微藻的毒性效应研究

设置不同浓度的重金属Cd2+(0、0.2、0.4、0.6、0.8和1 mg•L-1)和Pb2+(0、0.1、0.2、0. 4、0.8和1.6 mg•L-1)胁迫处理, 检测米氏凯伦藻(Karenia mikimotoi)的生长生理情况, 分析重金属胁迫对海洋微藻生长的毒性效应, 探讨超氧化物歧化酶(SOD)和过氧化氢酶(CAT)等对重金属胁迫的缓解作用。研究结果发现, 重金属Cd2+和Pb2+对米氏凯伦藻具有较强的毒性, 随着重金属浓度的提高, 细胞生长受到毒害作用增强; 而米氏凯伦藻对重金属Cd2+和Pb2+胁迫具有一定的适应性。重金属Cd2+和Pb2+胁迫导致米氏凯伦藻细胞的叶绿素a、叶绿素b含量下降(1.6 mg•L-1 Pb2+胁迫除外), 类胡萝卜素含量提高, 最大光能转化效率(Fv/Fm)下降, 表明重金属胁迫抑制藻的光合作用, 影响藻的生长繁殖。丙二醛(MDA)随着重金属Cd2+和Pb2+浓度提高而升高, 说明重金属引起藻细胞膜透性增加, 藻细胞遭受破坏。SOD活性整体呈现先升高后下降(或与对照持平)的趋势, 提示海洋微藻的抗氧化酶系统在低浓度重金属胁迫下产生应激性反应, 酶活性增强; 而CAT活性上升, 也对藻细胞起到保护作用, 推测两者共同反应, 以缓解藻体遭受的重金属毒害作用。结果可为了解重金属胁迫对海洋微藻的毒性效应提供参考。     

重金属Cd2+和Cu2+对一种曲壳藻生长情况及其抗氧化酶活性的影响

以淡水底栖硅藻曲壳藻(Achnanthes kryophila Petersen)为毒理试验材料, 研究了重金属镉、铜对曲壳藻生长及抗氧化酶活性的影响。结果表明: 镉和铜胁迫96 h EC50 分别为: 0.984 mgL–1 和1.589 mgL–1。藻生长量总体随重金属浓度的增加而降低, 然而镉(0-0.1 mgL–1)、铜(0-0.02 mgL–1)暴露组表现出明显的毒性兴奋效应。曲壳藻可溶性蛋白含量、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性随镉和铜胁迫浓度增加先升高后下降, 丙二醛(MDA)含量随着胁迫浓度增高逐渐增大, 镉和铜变化趋势大体相同, 但是变化幅度不同。高浓度重金属胁迫诱导氧自由基的大量产生,破坏了曲壳藻抗氧化酶系统的动态平衡, 加剧了膜脂过氧化作用, 影响藻细胞的生长并最终导致细胞死亡。     

一氧化氮(NO)对镉胁迫下小麦幼苗氧化损伤的影响

为探讨一氧化氮(NO)对重金属镉胁迫后小麦幼苗氧化损伤的影响。采用营养液水培法,以"晋麦8号"为材料,一氧化氮供体硝普钠(SNP),NO清除剂牛血红蛋白(Hb)及SNP类似物亚铁氰化钠(SF)分别处理小麦幼苗,研究NO在镉(Cd)胁迫下对小麦幼苗抗氧化系统的影响。结果显示,SNP处理可以缓解镉胁迫对幼苗生长抑制,显著增加可溶性蛋白、叶绿素和GSH含量,减少丙二醛(MDA)和过氧化氢(H2O2)的含量,并降低超氧阴离子(O2·-)产生速率、可溶性糖和脯氨酸的积累。而NO清除剂牛血红蛋白(Hb)处理使镉胁迫对小麦幼苗的毒害增强,SNP类似物亚铁氰化钠(SF)处理则没有缓解效应;进一步实验发现,SNP降低了镉胁迫下超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽还原酶(GR)和抗坏血酸过氧化物酶(APX)等抗氧化相关酶的活性,减轻了镉胁迫的氧化损伤。NO可以通过调节抗氧化酶系统来缓解Cd对植物的毒害。     

珙桐幼苗生理生化指标对重金属铅、镉胁迫的响应

铅和镉在土壤中表现出很强的毒性,严重危害植物的生长发育。该研究着眼于中国特有濒危珍稀植物珙桐,探究盆栽实验条件下其抗氧化酶活性、丙二醛(MDA)以及游离脯氨酸、可溶性蛋白对不同浓度重金属铅、镉胁迫的响应规律。结果表明:(1)不同浓度铅处理下,珙桐幼苗MDA浓度均显著高于对照组,而镉胁迫条件下除10 mg·kg~(-1)浓度外,其余处理组MDA浓度也显著高于对照组,表明了铅和镉污染加剧了珙桐膜脂过氧化进程。(2)游离脯氨酸随着铅、镉浓度的增加,表现出先增加后降低的现象,分别在铅浓度≥800 mg·kg~(-1)和镉浓度≥20 mg·kg~(-1)处理下显著低于对照组。可溶性蛋白浓度随着铅浓度的增加也表现出先增后减的规律,其浓度在镉胁迫下均显著高于对照组。可溶性蛋白和游离脯氨酸的增加可以提高珙桐抵抗低浓度重金属危害的能力,高浓度重金属对珙桐则产生抑制作用。(3)随着铅和镉浓度的增加,珙桐抗氧化酶活性也表现出先增加后降低的特征,表明了低浓度重金属(铅浓度≤600 mg·kg~(-1),镉浓度≤5mg·kg~(-1))容易激活珙桐抗氧化应激反应,有效地减少重金属的危害,高浓度的重金属则会抑制抗氧化酶活性。(4)通过相关性和主成分分析表明,珙桐幼苗中抗氧化酶、游离脯氨酸可以较好地反映珙桐对两种重金属胁迫的响应规律。     

微尼海双眉藻对重金属短期胁迫的生理及形态响应

为了探讨底栖硅藻微尼海双眉藻[Halamphora veneta(Kützing)Levkov]对重金属胁迫的响应机制,该研究分析了不同浓度的4种重金属Cu~(2+)、Hg~(2+)、Cd~(2+)和Pb~(2+)对微尼海双眉藻处理96h后,其细胞密度、叶绿素a含量、丙二醛含量以及形态结构的变化。结果显示:(1)低浓度的重金属处理会促进微尼海双眉藻的生长,而高浓度的重金属胁迫会抑制微尼海双眉藻的生长。(2)微尼海双眉藻叶绿素a对较低浓度的Cu~(2+)、Hg~(2+)、Cd~(2+)和Pb~(2+)胁迫均比较敏感,表明叶绿素a含量可以成为硅藻反映重金属含量的有效指标。(3)低浓度的重金属胁迫对微尼海双眉藻的丙二醛含量影响不明显,而高浓度的重金属胁迫会促进微尼海双眉藻的丙二醛含量显著升高。(4)Cu~(2+)、Cd~(2+)和Pb~(2+)胁迫不会引起微尼海双眉藻的明显细胞形变,而低浓度Hg~(2+)胁迫就会使微尼海双眉藻出现细胞膨大及畸形等变化。研究表明,微尼海双眉藻对于重金属胁迫具有某种耐受机制,其叶绿素a含量以及形态变化可以作为水体重金属污染的监测指标。     

植物重金属胁迫耐受机制

重金属是一类会对植物产生毒害作用的污染物,植物在长期进化过程中演变出耐受重金属胁迫的相关机制。以植物重金属耐受性为基础,对近几年来国内外植物响应重金属胁迫的耐受机制研究作一简要综述。主要概述了重金属对植物的胁迫影响及植物抗氧化系统,脯氨酸、可溶性糖、可溶性蛋白等渗透调节物质和不同类型基因家族等方面对植物耐受重金属胁迫机制的研究进展。以期为提高植物耐重金属胁迫能力及研究植物修复重金属污染土壤的应用奠定一定的基础。     

重金属Zn2+胁迫下米氏凯伦藻(Karenia mikimotoi)的生长生理响应研究

采用室内培养试验方法, 以米氏凯伦藻(Karenia mikimotoi)为生物材料, 设置不同浓度梯度的重金属Zn2+(0、1、5、10、15和20 mg•L-1), 主要测定藻细胞密度、光合色素、光合效率、抗氧化酶类、丙二醛(malondialdehyde, MDA)等相关指标, 探讨重金属Zn2+胁迫下米氏凯伦藻(Karenia mikimotoi)的生长和生理特征。结果发现, 在1和5 mg•L-1的Zn2+浓度下, 米氏凯伦藻细胞依然保持较好生长繁殖, 表明其具有一定的耐受性, 而随着重金属Zn2+浓度的提高, 细胞生长受到毒害抑制。光合色素含量呈现动态变化, 试验结束时(96 h)叶绿素a、叶绿素b和胡萝卜素含量有各自不同的变化趋势, 最大光能转化效率(Fv/Fm)表现出先升后降的趋势。Zn2+浓度为10 mg•L-1时, 超氧化物歧化酶(superoxide dismutase, SOD)活性显著高于对照; 过氧化氢酶(catalase, CAT)活性呈现出先上升后下降的趋势, 且5、10、15和20 mg•L-1 Zn2+浓度下米氏凯伦藻的过氧化氢酶(CAT)活性均显著高于对照; 10、15 mg•L-1 Zn2+浓度下米氏凯伦藻的总抗氧化能力(total antioxidant capacity, T-AOC)显著高于对照, 而20 mg•L-1 Zn2+浓度下的显著低于对照。丙二醛(MDA)呈现出随着Zn2+浓度提高而增加的趋势, 5、10、15和20 mg•L-1Zn2+浓度下米氏凯伦藻的丙二醛(MDA)均显著高于对照。结果可为了解重金属对海洋微藻的毒性作用提供数据参考。     

基于转录组分析重金属镉对长茎葡萄蕨藻的影响

随着人类社会工业化进程的加快,重金属镉(Cd)污染对海洋生物的毒害作用突显。为了探索Cd胁迫下长茎葡萄蕨藻生理调控的分子响应机制,本文采用RNA-Seq技术对镉胁迫(Hcd²⁺)藻体组织转录组进行研究。结果表明: 与对照相比,Hcd²⁺组共筛选出差异表达基因(DEGs)702个,其中,257个基因上调表达,445个基因下调表达。对获得的DEGs进行功能注释及富集分析,发现长茎葡萄蕨藻的多种生物学功能受到Cd²⁺胁迫的影响,最终表现为抑制生长。GO富集分析发现,长茎葡萄蕨藻体内氧自由基的产生与清除出现失衡,并产生了DNA损伤等氧化伤害。KEGG富集分析发现,长茎葡萄蕨藻中多条与光合作用相关途径受到抑制,表明Cd²⁺胁迫导致长茎葡萄蕨藻的光合反应紊乱。     

植物耐重金属的分子生物学研究进展

重金属污染对我国经济发展、人身健康造成重大负面影响,已经成为当今研究热点。综述了近年来重金属对植物的毒害及植物耐性机制等方面的研究进展,主要包括金属对植物的生长发育影响,植物抵抗重金属毒害的防御方式及抵抗重金属胁迫的相关基因和蛋白等,旨在为该领域的相关研究提供资料和借鉴。     

Cadmium stress: an oxidative challenge

At the cellular level, cadmium (Cd) induces both damaging and repair processes in which the cellular redox status plays a crucial role. Being not redox-active, Cd is unable to generate reactive oxygen species (ROS) directly, but Cd-induced oxidative stress is a common phenomenon observed in multiple studies. The current review gives an overview on Cd-induced ROS production and anti-oxidative defense in organisms under different Cd regimes. Moreover, the Cd-induced oxidative challenge is discussed with a focus on damage and signaling as downstream responses. Gathering these data, it was clear that oxidative stress related responses are affected during Cd stress, but the apparent discrepancies observed in between the different studies points towards the necessity to increase our knowledge on the spatial and temporal ROS signature under Cd stress. This information is essential in order to reveal the exact role of Cd-induced oxidative stress in the modulation of downstream responses under a diverse array of conditions.     

Cadmium decreases the levels of glutathione and enhances the phytochelatin concentration in the marine dinoflagellate <Emphasis Type="Italic">Lingulodinium polyedrum</Emphasis>

The toxic effects of metals on the aquatic environment are documented and well known. Metals are able to unbalance the intracellular redox potential and, therefore, induce the oxidative stress in living organisms. In this study, the responses of glutathione [reduced (GSH) and oxidized (GSSG)] and the structurally GSH-related peptides phytochelatins 3 and 4 (PC3 and PC4) were examined in the marine dinoflagellate Lingulodinium polyedrum exposed to cadmium (Cd). A novel method for PC3 and PC4 synthesis is described here based on a Boc strategy, yielding peptides with purities higher than 97 %. Analytical detection of GSH, GSSG, PC3, and PC4 applying liquid chromatography-tandem mass spectrometry (LC-MS/MS) method had been developed and described as robust and accurate with a detection limit of nmol g^?1 dry weight (DW) for PC3 and PC4. The intracellular levels of GSH and GSSG decreased dramatically over 24 and 48-h exposure to 18 μmol L^?1 Cd. These decreases were followed by the enhancement of intracellular PC3 and PC4 levels, in which syntheses started to be detected after 2 and 8-h exposure, respectively. Moreover, the PC4/PC3 ratio reached its maximum over 24-h exposure, being 8 to 75-fold higher than the one observed for other microalgae. This seems to be an efficient strategy of L. polyedrum to be protected against Cd environment contamination, since PC4 has more chelating sites and is structurally more stable than PC2 and PC3, the most abundant for other microalgae.     

产油微藻Auxenochlorella protothecoides UTEX 2341对镉胁迫的生理响应及抗性机理

【背景】重金属镉(Cd)污染问题日益严峻。微藻是一种良好的生物吸附剂。目前研究多关注于微藻对Cd的去除率及吸附性能方面,对其抗Cd机理的研究比较少。【目的】以产油微藻Auxenochlorella protothecoides UTEX 2341为材料,研究Cd胁迫对UTEX 2341生理性状、抗性机理及产油的影响。【方法】测定微藻在0-5mmol/LCd胁迫下的生长产油情况,并进一步分析2mmol/LCd胁迫下藻体中色素、可溶性蛋白和油脂含量的变化,以及藻体亚显微结构、抗氧化酶和抗氧化剂、脂肪酸组分的改变情况。【结果】Auxenochlorella protothecoides UTEX 2341能够耐受2 mmol/L Cd胁迫,虽然其生物量和叶绿素含量在Cd胁迫下略有降低,但油脂产量显著增加,胁迫168 h时为1.60 g/L,是对照的1.77倍。此外,高浓度Cd引起了胞内活性氧的积累。抗性机理分析表明高Cd胁迫显著抑制了微藻体内的抗氧化酶活性,但非酶抗氧化剂类胡萝卜素和还原性谷胱甘肽的含量显著增加,分别是对照的1.42倍和4.5倍,从而缓解高浓度Cd对微藻细胞造成的氧化损伤,减轻Cd的毒性。脂肪酸组分分析结果表明,Cd胁迫下油酸(C18:1)含量增加,且脂肪酸成分中C16-C18的含量达96%-98%,符合生物柴油的生产标准。【结论】该研究为揭示微藻抗Cd的机理以及Cd胁迫下微藻柴油合成的调控机理提供了一定的研究基础。     

Effect of cadmium on antioxidant enzyme activities and lipid peroxidation in the gills of the clam Ruditapes decussatus

Metals are known to influence the oxidative status of marine organisms, and antioxidant enzymes have been often proposed as biomarkers of effect. The clam Ruditapes decussatus is a well-known metal bioindicator. In this species cadmium (Cd) induces metallothionein (MT) synthesis only after 7 days of exposure. Before MT synthesis is induced, the other mechanisms capable of handling the excess of Cd are unknown. In order to identify some of these mechanisms, variations in antioxidant systems (superoxide dismutase, catalase, selenium-dependent glutathione peroxidase and non-selenium-dependent glutathione peroxidase), malondialdehyde (MDA) and MT were studied in the gills of R. decussatus exposed to different Cd concentrations (4, 40 and 100 gl^-1) for 28 days. These parameters, together with total proteins and Cd concentrations, were measured in the gills of the clams over different periods of exposure. Results indicate that Cd accumulation increased linearly in the gills of R. decussatus with the increase in Cd concentration. This increase induces an imbalance in the oxygen metabolism during the first days of Cd exposure. An increase in cytosolic superoxide dismutase (SOD) activity and a decrease in mitochondrial SOD activity was observed at the same time as or after a decrease in cytosolic and mitochondrial catalase activity and of selenium-dependent and non-selenium-dependent glutathione peroxidase activity. After 14 days of exposure, Cd no longer affect these enzymes but there was elevation of other cellular activities, such as MDA and MT production. MT bound excess Cd present in the cell. These variations in these parameters suggest their potential use as biomarkers of effects such as oxidative stress resulting from Cd contamination in molluscs.     

Effect of cadmium on antioxidant enzyme activities and lipid peroxidation in the gills of the clam Ruditapes decussatus

Metals are known to influence the oxidative status of marine organisms, and antioxidant enzymes have been often proposed as biomarkers of effect. The clam Ruditapes decussatus is a well-known metal bioindicator. In this species cadmium (Cd) induces metallothionein (MT) synthesis only after 7 days of exposure. Before MT synthesis is induced, the other mechanisms capable of handling the excess of Cd are unknown. In order to identify some of these mechanisms, variations in antioxidant systems (superoxide dismutase, catalase, selenium-dependent glutathione peroxidase and non-selenium-dependent glutathione peroxidase), malondialdehyde (MDA) and MT were studied in the gills of R. decussatus exposed to different Cd concentrations (4, 40 and 100 gl^-1) for 28 days. These parameters, together with total proteins and Cd concentrations, were measured in the gills of the clams over different periods of exposure. Results indicate that Cd accumulation increased linearly in the gills of R. decussatus with the increase in Cd concentration. This increase induces an imbalance in the oxygen metabolism during the first days of Cd exposure. An increase in cytosolic superoxide dismutase (SOD) activity and a decrease in mitochondrial SOD activity was observed at the same time as or after a decrease in cytosolic and mitochondrial catalase activity and of selenium-dependent and non-selenium-dependent glutathione peroxidase activity. After 14 days of exposure, Cd no longer affect these enzymes but there was elevation of other cellular activities, such as MDA and MT production. MT bound excess Cd present in the cell. These variations in these parameters suggest their potential use as biomarkers of effects such as oxidative stress resulting from Cd contamination in molluscs.     

活体微藻吸附水体中Cd2+的性能特征

【目的】藻类对重金属吸附和吸收是重金属进入食物链的重要渠道之一。研究活体微藻对水体中Cd~(2+)的吸附性能和吸附机理,旨在为Cd~(2+)等重金属离子进入水体后的去向及去除提供理论依据。【方法】选取地表水普遍存在的4种微藻:钝顶螺旋藻(Spirulina platensis)、铜绿微囊藻(Microcystis aeruginosa)、四尾栅藻(Scenedesmus quadricauda)和小球衣藻(Chlamydomonas microsphaera)作为试验材料,通过室内模拟实验,利用Langmuir、Freundlich和Dubinin-Radushkevich(D-R)3种等温吸附模型,研究4种活体微藻对Cd~(2+)的吸附规律及吸附参数。【结果】4种微藻对水体Cd~(2+)吸附均可以用Langmuir、Freundlich和D-R模型描述,其中用Langmuir模型拟合钝顶螺旋藻、Freundlich模型拟合小球衣藻、D-R模型拟合铜绿微囊藻和四尾栅藻的吸附效果最佳。四尾栅藻对Cd~(2+)的吸附量最高,而钝顶螺旋藻对Cd~(2+)的吸附量最低,但与Cd~(2+)的亲和力最强,4种微藻吸附Cd~(2+)主要是以离子代换为主的化学吸附。【结论】微藻对Cd~(2+)均有较强的吸附能力,会引起以微藻为食的水生动物Cd~(2+)富集;微藻也是去除水体Cd~(2+)的潜在吸附剂原料。     

Metabolic networks to combat oxidative stress in Pseudomonas fluorescens

Oxidative stress is an unavoidable peril that aerobic organisms have to confront. Thus, it is not surprising that intricate strategies are deployed in an effort to fend the dangers associated with living in an O(2) environment. In the classical models of anti-oxidative defense mechanisms, a variety of stratagems including the reactive oxygen species (ROS) scavenging systems, the NADPH-generating enzymes and the DNA repair machineries are highlighted. However, it is becoming increasingly clear that metabolism may be intimately involved in anti-oxidative defence. Recent data show that metabolic reprogramming plays a pivotal role in the survival of organisms exposed to oxidative stress. Here, we describe how Pseudomonas fluorescens, the metabolically-versatile soil microbe, manipulates its metabolic networks in an effort to counter oxidative stress. An intricate link between metabolism and anti-oxidative defense is presented. P. fluorescens reconfigures its metabolic processes in an effort to satisfy its need for NADPH during oxidative insult. Seemingly, disparate metabolic modules appear to partner together to concomitantly fine-tune the levels of the anti-oxidant NADPH and the pro-oxidant NADH. Central to this shift in the metabolic production of the pyridine nucleotides is the increase in NAD kinase with the concomitant decrease in NADP phosphatase. The tricarboxylic acid cycle is tweaked in an effort to limit the formation of NADH. This metabolic redox-balancing act appears to afford a potent tool against oxidative challenge and may be a more widespread ROS-combating tactic than hitherto recognized.     

脂肪组织氧化应激与运动干预

脂肪组织在调控代谢稳态和运动适应中扮演着重要的角色。肥胖引起的脂肪组织氧化应激是2型糖尿病与代谢综合征等的重要病理特征,是促进脂肪组织炎症和胰岛素抵抗的重要机制。氧化应激可以引起脂肪细胞趋化因子表达,募集炎症细胞浸润脂肪组织,炎症细胞分泌大量的炎症因子,并促进了局部和系统的胰岛素抵抗与慢性炎症。运动对肥胖相关的慢性代谢病的有效干预与运动的抗氧化效应相关。本文总结了氧化应激在脂肪组织炎症和胰岛素抵抗中的作用,以及运动对脂肪组织氧化应激的调控。     

镉毒害下植物氧化胁迫发生及其信号调控机制的研究进展

土壤重金属污染引发了一系列严峻的环境问题.其中,镉(Cd)是生物毒性最强的重金属元素之一.活性氧(ROS)过量积累引起的氧化胁迫,是Cd毒害植物的主要原因之一.本文围绕Cd胁迫引起的ROS积累及清除过程,重点阐述介导上述过程的一些信号调控物质包括一氧化氮(NO)、钙(Ca)、植物激素如生长素(IAA)和脱落酸(ABA)等及有丝分裂原活化蛋白激酶(MAPKs)的变化及其在缓解Cd诱导的氧化胁迫中的作用,以期为今后植物抗Cd胁迫生理生化机制的研究提供一定的理论依据.     

Differential pattern of Cu/Zn superoxide dismutase isoforms in relation to tidal spatio-temporal changes in the blue mussel Mytilus edulis

Inducible antioxidant defences in marine organisms such as mussel bivalves are commonly used as biomarkers of pollutant-induced oxidative stress and their variations proposed as one of the biological effect measurements for assessment of contamination impact in aquatic environments. Among them, the copper/zinc superoxide dismutases (Cu/Zn-SODs) are metalloenzymes which play a key role in the protection of cells in case of oxidative stress. In order to observe possible variations of an antioxidant response in relation to tidal oscillations, the copper/zinc superoxide dismutase activity (Cu/Zn-SOD) was characterized in the digestive gland and gills of blue mussels sampled at high and low shore throughout the tidal cycle. Determination of SOD activity was performed on gels after isoelectro-focusing, allowing the revelation of three isoforms. In both tissues, high-shore mussels exhibited a higher level of total SOD activity than low-shore mussels. During emersion, a decrease of total SOD activity appeared in digestive gland for both groups. In high-shore mussels, the less acidic form contributed to 75% of the total activity, the second one to 20% and the more acidic one to 5% in both tissues before air exposure. During emersion, the relative contribution of the three isoforms to the total activity was markedly changed with a significant decrease in intensity of the first isoform and parallel increases in the two other ones. After re-immersion a progressive recovery of proportions of SOD isoforms was observed. In low-shore mussels, the relative contribution of the three isoforms to the total SOD activity showed similar changes. The observed variations could correspond to changes in the redox status of the mussels during tidal oscillations.