Effects of thermal stress and nickel exposure on biomarkers responses in Mytilus galloprovincialis (Lam).

The present work aimed to assess the Mytilus galloprovincialis digestive gland biomarkers responses to nickel (Ni) exposure along with a heat stress gradient. Mussels were exposed to a sublethal dose of nickel (13 µM) along with a temperature gradient (18 °C, 20 °C, 22 °C, 24 °C and 26 °C) for 4 days. Metallothionein (MTs) content was assessed as specific response to metals. Catalase (CAT), glutathione S-transferase (GST) activities and malondialdehyde (MDA) were measured as biomarkers of oxidative stress and lipid peroxidation. The cholinergic system was monitored using the acetylcholinesterase activity (AChE). Moreover, Ni uptakes along with the exposure temperatures were assessed. A correlation matrix (CM) between the investigated biomarkers and the exposure temperatures and a Principal Component Analysis (PCA) were achieved. Our data showed a negative effect of temperature increase on mussel's antioxidant and detoxification response to Ni exposure being more pronounced in animals exposed to the 24 °C and 26 °C.

Increased temperatures affect oxidative stress markers and detoxification response to benzo[a]pyrene exposure in mussel Mytilus galloprovincialis.

The present research work was designed to study mussel's (Mytilus galloprovincialis) digestive gland biotransformation and detoxification responses to benzo[a]pyrene (B[a]P) exposure along with heat stress. Mussels were exposed to a sublethal dose of B[a]P [75 nM (19 µg/L/animal)] + temperature gradient (18, 20, 22, 24 and 26 °C) for 7 days. B[a]P hydroxylase (BPH) and glutathione-S-transferase (GST) activities were assessed in digestive gland tissues as phase I and phase II biotransformation parameters. Catalase (CAT) activity and malonedialdehyde (MDA) were measured as potential biomarkers of oxidative stress and lipid peroxidation. The cholinergic system was evaluated using acetylcholinesterase (AChE) activity. DNA damage was assessed using micronuclei (MN) test. BPH and GST activities showed a decreasing trend in B[a]P-exposed animals at 24 and 26 °C. CAT activity showed a bell-shaped response in B[a]P-exposed and in heat-stressed organisms at a maximum temperature of 22 °C. AChE activity was significantly inhibited in response to B[a]P being more pronounced at a temperature of 26 °C. MN in digestive gland cells suggest that B[a]P exposure induced significant DNA alteration with a maximum response in organisms coexposed to B[a]P and a temperature of 26 °C. Biomarker data are further discussed in relation B[a]P accumulation in mussels digestive gland. These data should be carefully considered in view of the biological effects of organic pollutants, particularly in organisms under the challenging effects of extreme temperature fluctuations.

Uptake and biochemical responses of mussels Mytilus galloprovincialis exposed to sublethal nickel concentrations.

In the present study, mussel (Mytilus galloprovincialis) digestive gland oxidative stress biomarkers and detoxification responses to acute exposure to nickel (Ni) were investigated. Mussels were exposed to two sublethal concentrations of Ni (135 µg/L per animal (2.5 µM) and 770 µg/L per animal (13 µM)) for 24, 48, 72, 96 h and 8 days. Following biological responses were measured: (1) glutathione S-transferase (GST) activity as a phase II conjugation enzyme, (2) catalase activity as antioxidant response, (3) malondialdehyde accumulation (MDA) as lipid peroxydation marker and metallothionein as specific response to metals exposure. The cholinergic system was evaluated using the acetylcholinesterase activity (AChE). Moreover, Ni uptakes during the exposure periods were assessed and the uptake rate constant determined. A correlation matrix (CM) between the investigated biomarkers and a principal component analysis (PCA) were achieved for the two tested concentrations. The Ni-uptake constant was higher in animals exposed to the lowest concentration. The CM and the PCA showed a time-dependent effect of the Ni exposure on the investigated biomarkers being more pronounced in animals exposed to the highest Ni concentration. While AChE showed a significant increase after 48 h and a further return to control values in the lowest concentration, it was drastically maintained inhibited in the highest concentration. Our data provided clues about the occurrence of different toxicokinetics and toxicodynamics of two Ni sublethal concentrations in an ecologically relevant organism.