Ascorbic acid protects Coccomyxa subellipsoidea against metal toxicity through modulation of ROS/NO balance and metal uptake

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14310%2F17%3A00097366" target="_blank" >RIV/00216224:14310/17:00097366 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1016/j.jhazmat.2017.06.035" target="_blank" >http://dx.doi.org/10.1016/j.jhazmat.2017.06.035</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.jhazmat.2017.06.035" target="_blank" >10.1016/j.jhazmat.2017.06.035</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Ascorbic acid protects Coccomyxa subellipsoidea against metal toxicity through modulation of ROS/NO balance and metal uptake

Popis výsledku v původním jazyce

Impact of exogenous ascorbic acid (AsA, 100 uM) on acute metal toxicity (Pb and Hg, 24 h of exposure to 100 uM) in unicellular green alga Coccomyxa subellipsoidea was studied. Hg (often extensively) depleted amount of pigments, potassium, soluble proteins, endogenous AsA, non-protein thiols and nitric oxide signal but elevated ROS signal and activities of catalase and superoxide dismutase. Responses to Pb application (if any) were less visible with ROS signal being slightly elevated and amount of non-protein thiols being slightly reduced. Exogenous AsA considerably improved mainly Hg-induced damage at the level of oxidative stress and physiological parameters and evoked an increase in nitric oxide signal. Maximum amount of total Hg was almost 4-fold higher than that of Pb (36.5 vs. 9.73 mg/g DW) and AsA depleted both total and intracellular accumulation. At the level of ascorbate-related proteins, exogenous AsA suppressed metal-induced expression and activity of MDHAR and APX but not of DHAR, which may indicate a role of DHAR in algal stress tolerance. Our data suggest that given Coccomyxa species is suitable candidate for remediation of Hg or Pb and that ascorbic acid effectively ameliorates metal-induced toxicity without side effects.

Název v anglickém jazyce

Ascorbic acid protects Coccomyxa subellipsoidea against metal toxicity through modulation of ROS/NO balance and metal uptake

Popis výsledku anglicky

Impact of exogenous ascorbic acid (AsA, 100 uM) on acute metal toxicity (Pb and Hg, 24 h of exposure to 100 uM) in unicellular green alga Coccomyxa subellipsoidea was studied. Hg (often extensively) depleted amount of pigments, potassium, soluble proteins, endogenous AsA, non-protein thiols and nitric oxide signal but elevated ROS signal and activities of catalase and superoxide dismutase. Responses to Pb application (if any) were less visible with ROS signal being slightly elevated and amount of non-protein thiols being slightly reduced. Exogenous AsA considerably improved mainly Hg-induced damage at the level of oxidative stress and physiological parameters and evoked an increase in nitric oxide signal. Maximum amount of total Hg was almost 4-fold higher than that of Pb (36.5 vs. 9.73 mg/g DW) and AsA depleted both total and intracellular accumulation. At the level of ascorbate-related proteins, exogenous AsA suppressed metal-induced expression and activity of MDHAR and APX but not of DHAR, which may indicate a role of DHAR in algal stress tolerance. Our data suggest that given Coccomyxa species is suitable candidate for remediation of Hg or Pb and that ascorbic acid effectively ameliorates metal-induced toxicity without side effects.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30304 - Public and environmental health

Projekt

—

Návaznosti

S - Specificky vyzkum na vysokych skolach

Rok uplatnění

2017

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

JOURNAL OF HAZARDOUS MATERIALS

ISSN

0304-3894

e-ISSN

—

Svazek periodika

339

Číslo periodika v rámci svazku

October

Stát vydavatele periodika

NL - Nizozemsko

Počet stran výsledku

8

Strana od-do

200-207

Kód UT WoS článku

000407188200021

EID výsledku v databázi Scopus

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