Toxicity of selenite in the unicellular green alga Chlamydomonas reinhardtii: Comparison between effects at the population and sub-cellular level

Morlon, Hélène; Fortin, Claude; Floriani, Magali; Adam, Christelle; Garnier‐Laplace, Jacqueline; Boudou, A.

doi:10.1016/j.aquatox.2005.02.007

Cited by 75 publications

(45 citation statements)

References 36 publications

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“…5). Similar responses were also found in Chlamydomonas reinhardtii and Chlorella pyrenoidosa upon exposure to heavy metals (Morlon et al 2005;Liu and Xiong 2009). Our results were in agreement with these findings.…”

Section: Tpt Induced Oxidative Stress and Antioxidative Responses In supporting

confidence: 72%

“…Living organisms utilize various defense mechanisms such as intracellular detoxification, sequestration and/or assimilative reduction to resist the exposure of toxicants (Morlon et al 2005). Superoxide dismutase (SOD, EC.1.15.1.1), glutathione peroxidase (GPx, EC.1.11.1.9) and catalase (CAT, EC.1.11.1.6) form the first-line of enzymatic defense against ROS in the cells and their increased activities have been widely adopted to indicate the presence of oxidative stress and the ability of the cell to scavenge ROS.…”

Section: Introductionmentioning

confidence: 99%

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Triphenyltin induced growth inhibition and antioxidative responses in the green microalga Scenedesmus quadricauda

Mak

et al. 2010

Ecotoxicology

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The toxicity of organotin compounds in the environment is closely related to their uptake by microorganisms and delivery through the food chain. The population at low trophic levels like microalgae plays an important role in this aspect. In this study, the toxic effects of triphenyltin (TPT) on Scenedesmus quadricauda were assessed at the population, cellular and subcellular levels. The alga was exposed to TPT of up to 64 μg l(-1) (nearly lethal concentration), but the algal growth was inhibited significantly when TPT was elevated to 8 μg l(-1). This growth inhibition was correlated to the presence of oxidative stress as evidenced by the accumulation of malondialdehyde (MDA) and confirmed by fluorescent probing of the intracellular reactive oxygen species (ROS) levels. The imbalanced activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) may lead to an accumulation of intracellular H(2)O(2), which can initiate an oxidative damage to cell components and cause growth inhibition and finally cell death. The detachment of plasma membrane from cell wall, the structural change of chloroplasts as well as the increased number and size of starch granules together with electron-dense deposits in chloroplasts were noticed through electron microscopic examination. It was suggested that mitochondria, chloroplasts and protoplasm might be the direct targets of TPT toxicity. This study confirmed that TPT poisoning on phytoplankton can happen at very low concentrations. There existed different defense mechanisms e.g., antioxidant enzyme activation, starch accumulation and possibly metal sequestration in algal species as the means to resist TPT toxicity.

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Section: Tpt Induced Oxidative Stress and Antioxidative Responses In supporting

confidence: 72%

Section: Introductionmentioning

confidence: 99%

Triphenyltin induced growth inhibition and antioxidative responses in the green microalga Scenedesmus quadricauda

Mak

et al. 2010

Ecotoxicology

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“…Selenium is considered an essential micronutrient in algae and some plants and animals; however, at doses only 100 times greater than required, Se begins to cause toxic effects in some sensitive biological species, including mostly oviparous vertebrates [7][8][9]. In algae, selenite is known to cause damage to chloroplasts, specifically in the stroma, thylakoid, and pyrenoid [10].…”

Section: Introductionmentioning

confidence: 99%

Phytochelatin induction by selenate in Chlorella vulgaris, and regulation of effect by sulfate levels

Simmons

Emery

2010

Enviro Toxic and Chemistry

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Phytochelatins (PCs) are short metal detoxification peptides made from the sulfur-rich molecule glutathione. The production of PCs by algae caused by Se exposure has never been studied, although many algae accumulate Se, forming Se-rich proteins and peptides, and higher plants have demonstrated PC production when treated with Se; therefore, a goal of the current study was to examine whether Se induces PC production in algae. Furthermore, selenate is thought to compete with sulfate in the S assimilation pathway, and sulfate therefore may have a protective effect against the toxic effects of high doses of Se in algae. Hence, the interaction of selenate and sulfate was investigated with respect to the induction of PCs. Chlorella vulgaris was cultured in media with either low (31.2 µM) or high (312 µM) concentrations of sulfate. These cultures were exposed to selenate in doses of 7, 35, and 70 nM for 48 h. In a separate treatment, Cd (890 nM) was added as a positive PC-inducing control, and one no-metal negative control was used. Total Se and Se speciation were determined, and glutathione, phytochelatin-2, and phytochelatin-3 were quantified in each of cell digests, cell medium, and cell lysates. We found that PCs and their precursor glutathione were induced by selenate as well as by a Cd control. The high concentration of sulfate was able to counter selenate-induced production of PCs and glutathione. These data support two possible mechanisms: a negative feedback system in the S assimilation pathway that affects PC production when sulfate is abundant, and competition for uptake at the ion transport level between selenate and sulfate.

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“…Our TEM analysis showed that dichloromethane and dichloroethane increased the number of starch granules. An increase in starch content was also observed by Morlon et al (2005), who showed that starch granules were overproduced by algae in response to selenite exposure. TEM also showed that dichloromethane and dichloroethane partially damaged the structure of chloroplasts, and this could be observed visually, as cells turned from green to white when exposed to dichloromethane and dichloroethane observed in this study.…”

Section: Discussionmentioning

confidence: 74%

Toxicological Responses ofChlorella vulgaristo Dichloromethane and Dichloroethane

Zhang

et al. 2014

Environmental Engineering Science

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The aim of this study was to evaluate the acute toxicity effects of dichloromethane and dichloroethane on Chlorella vulgaris at the physiological and molecular level. Data showed that the cell number, chlorophyll a, and total protein content gradually decreased with increasing dichloromethane and dichloroethane concentrations over a 96-h exposure. Lower doses of two organic solvents had stimulatory effects on catalase and superoxide dismutase activity. Malondialdehyde showed a concentration-dependent increase in response to dichloromethane and dichloroethane exposure. Electron microscopy also showed that there were some chloroplast abnormalities in response to different concentrations of dichloromethane and dichloroethane exposure. Real-time polymerase chain reaction assay demonstrated that dichloromethane and dichloroethane reduced the transcript abundance of psaB, whereas that of psbC changed depending on the toxicant after 24 h of exposure. Dichloromethane and dichloroethane affected the activity of antioxidant enzymes, disrupted the chloroplast ultrastructure, and reduced transcription of photosynthesis-related genes in C. vulgaris, leading to metabolic disruption and cell death.

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Toxicity of selenite in the unicellular green alga Chlamydomonas reinhardtii: Comparison between effects at the population and sub-cellular level

Cited by 75 publications

References 36 publications

Triphenyltin induced growth inhibition and antioxidative responses in the green microalga Scenedesmus quadricauda

Triphenyltin induced growth inhibition and antioxidative responses in the green microalga Scenedesmus quadricauda

Phytochelatin induction by selenate in Chlorella vulgaris, and regulation of effect by sulfate levels

Toxicological Responses ofChlorella vulgaristo Dichloromethane and Dichloroethane

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