Deleterious effect of Chattonella marina on short-necked clam (Ruditapes philippinarum); possible involvement of reactive oxygen species

In laboratory exposure experiments, Chattonella marina showeda deleterious effect on short-necked clams (Ruditapes philippinarum).Accumulated C. marina cells were observed in gill tissues ofthe clams exposed to C. marina. Immunohistochemical analysisusing antiserum against the crude glycocalyx of C. marina suggestedthat the glycocalyx was present on the gill surface. Mucus substancesprepared from gill tissue of the clams stimulated C. marinato generate increased amounts of O₂^– in a concentration-dependentmanner. These results suggest that reactive oxygen species (ROS)-mediatedgill tissue damage is one of the causative factors responsiblefor the harmful effect of C. marina on shellfish.     

Effects of lethal levels of environmental hypercapnia on cardiovascular and blood-gas status in yellowtail,Seriola quinqueradiata

The cardiorespiratory responses were examined in yellowtail, Seriola quinqueradiata exposed to two levels of hypercapnia (seawater equilibrated with a gas mixture containing 1% CO(2) (water PCO(2) = 7 mmHg) or 5% CO(2) (38 mmHg)) for 72 hr at 20 degrees C. Mortality was 100% within 8 hr at 5% CO(2), while no fish died at 1% CO(2). No cardiovascular variables (cardiac output, Q; heart rate, HR; stroke volume, SV and arterial blood pressure, BP) significantly changed from pre-exposure values during exposure to 1% CO(2). Arterial CO(2) partial pressure (PaCO(2)) significantly increased (P < 0.05), reaching a new steady-state level after 3 hr. Arterial blood pH (pHa) decreased initially (P < 0.05), but was subsequently restored by elevation of plasma bicarbonate ([HCO(3)(-)]). Arterial O(2) partial pressure (PaO(2)), oxygen content (CaO(2)), and hematocrit (Hct) were maintained throughout the exposure period. In contrast, exposure to 5% CO(2) dramatically reduced Q (P < 0.05) through decreasing SV (P < 0.05), although HR did not change. BP was transiently elevated (P < 0.05), followed by a precipitous fall before death. The pHa was restored incompletely despite a significant increase in [HCO(3)(-)]. PaO(2) decreased only shortly before death, whereas CaO(2) kept elevated due to a large increase in Hct (P < 0.05). We tentatively conclude that cardiac failure is a primary physiological disorder that would lead to death of fish subjected to high environmental CO(2) pressures.