Estuarine and intertidal bivalve mollusks frequently experience salinity fluctuations that may drive oxidative stress (OS) in the organism. Here we investigated OS markers and histopathological changes in gills and hemolymph of Mediterranean mussels Mytilus galloprovincialis acclimated to a wide range of salinities (6, 10, 14, 24, and 30 ‰). Mussels were captured at the shellfish farm with the salinity of 18% and then acclimated to hypo- and hypersaline conditions in the laboratory at the speed of 1.5±0.5‰ per day. Indicators of redox balance in hemocytes (intracellular reactive oxygen species (ROS) levels, DNA damage) and gills (thiobarbituric acid reactive substances (TBARS), protein carbonyls (PC), activity of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) were measured. The results revealed induction of OS in tissues and cells of mussels for both experimental increase and decrease salinity modeling. Hemocytes showed higher sensitivity to oxidative damage from salinity stress compared to gills, as DNA damage and elevated ROS levels were observed in all experimental groups except 14‰. A decrease in environmental salinity to 10 ‰ was likely within the physiological norm for mussels, as minor oxidative damage was noted. At a salinity of 6 ‰, the most significant signs of redox imbalance, including DNA damage, increased ROS production levels in hemocytes, and suppressed activity of SOD in gills were observed, along with elevated PC levels. An increase in environmental salinity up to 30 ‰ led to the enhancement of the activity of antioxidant enzymes in the gills, which may be attributed to the high capacity of the antioxidant system in this organ. The study provides new insights into the effects of salinity stress on the tissue and cellular redox balance of bivalves, which is crucial for better understanding the potential consequences of the global transformation of coastal ecosystems.

The impairment of mitochondrial respiration, observed in neurodegenerative and cardiovascular disease, diabetes, cancer, and migraine headaches, has emerged as a biomarker of mitochondrial dysfunctions. Chronic fatigue, depression, and other behavior/mood disorders are also associated with mitochondrial malfunctioning, but so is our lifestyle! Our lab offers tests for insight into mitochondrial fitness, linking not only diseases but also behaviors and modern lifestyles that lead to health damage. Firstly, we focused on 88 (relatively) healthy volunteers, of which 32% were taking some medication (such as for high blood pressure or mood disorders), however, they considered themselves fit and healthy.  The blood was drawn 3h before PBMC (peripheral blood mononuclear cells) isolation, followed by an immediate Seahorse XF Cell Mito Stress Test (Agilent) on the SeahorseXF96e instrument (Agilent). Parameters of mitochondrial respiration were carefully examined. There was a significant difference between BHI (bioenergetic health index), reserve capacity, coupling efficiency, and proton leak, between people who took medication for chronic but manageable comorbidities and completely healthy individuals. Later, in another group we examined the alterations in NAD+ levels (by Q-NADMED Blood NAD+ assay kit, NADMED) and mitochondrial respiration parameters in a binge-drinking session (consuming 10 or more units of alcohol in less than three days). The decrease in NAD+ levels was positively correlated with the amount of alcohol consumed. Additionally, total NAD+ levels positively correlated with the BHI.  In another experiment, supplementation with niacin for 20 days, did not increase NAD+ levels in (relatively) healthy individuals. Apart from mitochondrial respiration and NAD+ levels, we focus on optimizing tests for mtDNA count and mitochondrial potential. All of these tests not only explore disease but also serve to monitor behaviors that lead to health damage or improvements.