Hypoxia tolerance and physiological coping strategies in fat greenling (Hexagrammos otakii).

Abstract

Dissolved oxygen (DO) is necessary for fish survival and growth. This study investigated the hypoxia tolerance, hematological indexes, hepatic antioxidant capacity, and liver and gill morphological alternation of fat greenling during hypoxia stress. Changes in hematological parameters (cortisol, glucose, lactic acid, hemoglobin [Hb], hematocrit [Hct], and white blood cell [WBC], and red blood cell [RBC] numbers), hepatic antioxidant enzymes (superoxide dismutase [SOD], glutathione peroxidase [GSH-Px], catalase [CAT]), aminotransferase (AST), alanine aminotransferase (ALT) activities, and malondialdehyde (MDA) contents, and the histology of the liver and gill were evaluated under hypoxia stress and reoxygenation. Results showed that the DO at critical oxygen tension (Pcrit) and loss of equilibrium (LOE) were 3.10 ± 0.17 mg/L and 1.90 ± 0.11 mg/L, respectively. Hypoxia stress significantly stimulated the respiratory frequency rate, Hb and Hct levels, and RBC numbers; the highest values were observed at Pcrit and LOE, respectively. Serum glucose, cortisol and lactic acid contents, and hepatic MDA, AST, ALT, SOD, and CAT activity demonstrated similar results to Hb. However, hepatic GSH-Px activity obtained the highest value at Pcrit and drastically decreased the lowest value at LOE. Moreover, hypoxia stress induced hepatocyte necrosis, vacuolization, and increased hepatocyte apoptosis rate. Lamellar perimeters, length, surface area, and gill surface area manifested results similar to those for respiratory frequency rate, whereas lamellar width and interlamellar distance significantly decreased at Pcrit, LOE, and reoxygenation treatment for 4 h. The above parameters returned to nearly normal levels after reoxygenation treatment for 8 h. These results suggest that fat greenling is a hypoxia-tolerant marine fish that copes with potential hypoxia-induced damage by elevating hematological-related parameters, stimulating hepatic antioxidant capacity, and altering the gill and liver morphology to maintain homeostasis.