Redox Homeostasis Disclosed in the Saltmarsh Plant Halimione portulacoides upon Short Waterborne Exposure to Inorganic Mercury

Author:

Pereira Patrícia1ORCID,Pereira Joana Luísa1ORCID,Marques Ana1,Marques Carlos1,Brandão Fátima1ORCID,Cesário Rute2ORCID,Frankenbach Silja1ORCID,Serôdio João1,Gonçalves Fernando J. M.1ORCID,Canário João2ORCID,Pacheco Mário1ORCID

Affiliation:

1. CESAM and Department of Biology, University of Aveiro, 3810-193 Aveiro, Portugal

2. Centro de Química Estrutural, Institute of Molecular Sciences and Department of Chemical Engineering, Instituto Superior Técnico, Universidade de Lisboa, 1049-001 Lisboa, Portugal

Abstract

The saltmarsh plant Halimione portulacoides was shortly exposed to realistic levels of inorganic mercury (iHg) with the aim of investigating the adaptative processes of the roots and leaves regarding redox homeostasis, physiology, and Hg accumulation. Plants were collected at a contaminated (CONT) and a reference (REF) site to address the interference of contamination backgrounds. The influence of major abiotic variables (i.e., temperature and light) was also examined. Total Hg levels, antioxidant enzymes, lipid peroxidation (LPO), and photosynthetic activity were analyzed after 2 and 4 h of exposure. A poor accumulation of Hg in the roots was noticed, and no translocation to the stems and leaves was found, but plants from the CONT site seemed more prone to iHg uptake (in winter). Despite this, antioxidant modulation in the roots and leaves was found, disclosing, in winter, higher thresholds for the induction of enzymatic antioxidants in CONT leaves compared to REF plants, denoting that the former are better prepared to cope with iHg redox pressure. Consistently, CONT leaves exposed to iHg had remarkably lower LPO levels. Exposure did not impair photosynthetic activity, pinpointing H. portulacoides’ ability to cope with iHg toxicity under very-short-term exposure. Biochemical changes were noticed before enhancements in accumulation, reinforcing the relevance of these responses in precociously signaling iHg toxicity.

Funder

FCT

National funds

Publisher

MDPI AG

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