Activity of Energy Metabolism Enzymes and ATP Content in the Brain and Gills of the Black Sea Scorpionfish Scorpaena porcus under Short-Term Hypoxia

Abstract

The effect of short-term hypoxia on the activity of oxidoreductases, malate dehydrogenase (MDH, 1.1.1.37) and lactate dehydrogenase (LDH, 1.1.1.27) responsible for urgent adaptation to oxygen deficiency, was studied in the brain and gills (first branchial arch) of the Black Sea scorpionfish Scorpaena porcus. The control group of fish was kept at 4.5–6.7 mg O2 L–1 (normoxia), experimental groups were exposed to 1.7–3.7 mg O2 L–1 (mild hypoxia) and 0.3–1.0 mg O2 L–1 (acute hypoxia); the exposure time was 90 min, water temperature 21–22°C. The dissolved oxygen level was reduced by saturating water with nitrogen. Hypoxia had no significant impact on the brain structures. Under acute hypoxia, MDH and LDH activities, the MDH/LDH index and ATP level in the forebrain, diencephalon and midbrain (FDMB), as well as in the medulla oblongata (MB), remained at the level of control values. Mild hypoxia caused a proportional rise in MDH and LDH activities and an increase in the ATP level in FDMB, most likely, due to a reduced demand for ATP in this brain region. This phenomenon is supposed to be based on the GABAergic mechanism of brain activity regulation, which is able to reduce energy demands of nervous tissue due to increasing the GABAA receptor density. The gills were distinguished by minimum MDH and LDH activities at the background of high MDH/LDH index values. Acute hypoxia led to decrease LDH activity and increase the MDH/LDH index in the gills, reflecting thereby a transition of this organ to an anaerobic operational mode. Under acute hypoxia, there was detected an increase in the relationship within the “MDH activity ↔ LDH activity” system in all types of tissues (r = 0.81–0.94, p < 0.05–0.01), which is typical of the species tolerant to oxygen deficiency. Apparently, this effect is based on MDH coupling with glycolytic substrates under conditions of acute oxygen deficiency, which rules out excessive lactate accumulation under metabolic depression.