Abstract

A unicellular cyanobacterium Synechococcus elongatus PCC 7942 was exposed to various concentrations of SeO42–. A growth supportive effect was seen at 50 µM concentration of SeO42− whereas 50% growth retardation was observed at 200 µM of SeO42−. Selenium (Se) stress at 200 µM SeO42− induced the formation of reactive oxygen species such as superoxide radical (O2•–), hydrogen peroxide (H2O2) and malondialdehyde (MDA). Modifications in antioxidant enzyme levels, namely, superoxide dismutase (SOD), catalase (CAT), peroxidase (POX), glutathione reductase (GR), glutathione peroxidase (GPX) and isozyme patterns were also examined. This article outlines the synergistic action of antioxidant components on Se toxicity in S. elongatus PCC 7942. Key words: Antioxidant, reactive oxygen species, selenium, Synechococcus elongatus PCC 7942, toxicity.

Highlights

  • In freshwaters, selenium (Se) entering primarily as selenate (SeO42–) and selenite (SeO32–) oxyanions has high bioavailability and exert their toxicities

  • In order to study the effect of Se on the growth of unicellular cyanobacterium S. elongatus PCC 7942, culture was grown in BG-11 medium in the absence and presence of various concentration SeO42− (50 to 500 μM)

  • SeO42− has either stimulating or toxic effects on the culture of S. elongatus PCC 7942 depending on the Se levels in BG-11 medium

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Summary

Introduction

Selenium (Se) entering primarily as selenate (SeO42–) and selenite (SeO32–) oxyanions has high bioavailability and exert their toxicities. Se act as beneficial element by boosting normal cell growth and function as observed in plants at low doses (Feng and Wei, 2012). At high doses Se is toxic to algae, leading to reduction of growth rate or alterations in the levels of reactive oxygen species (ROS) (Arauz et al, 2016). These ROS involve superoxide radical (O2–), hydrogen peroxide (H2O2) and hydroxyl radical (.OH) that may cause oxidation of nucleic acids and proteins as well as lipid peroxidation (LPO), leading further to inactive enzymes, disrupted membranes, mutations, and causing cell death (Schiavon et al, 2012)

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