Effect of Chattonella Exposure on Acid-Base Status of the Yellowtail.

Abstract

The effect of Chattonella exposure on the acid-base status of the yellowtail Seriola quinqueradiata was analyzed to assess the validity of the hypothesized mechanism of fish kill by this plankton species. Based on the finding that gill carbonic anhydrase was inactivated in fish exposed to Chattonella, it was hypothesized that this inactivation resulted in certain physiological disorders such as decreases in blood pH and Po2. None of the acid-base variables measured in this study (arterial blood pH (pHe), red blood cell intracellular pH (pHi), Pco2 (Paco2), and total CO2 of plasma (Taco2p)) varied substantially from their control values after the onset of exposure except for some increases in pHi. It was only the terminal blood samples that demonstrated sharp decreases in pHe and pHi and elevation of Paco2. In contrast, arterial Po2 decreased rapidly after the onset of plankton exposure. Overall these results do not support the above hypothesis.

The Effects of Harmful Algal Blooms on Aquatic Organisms

“…A decrease in the oxygen partial pressure of arterial blood and an increase in plasma catecholamines are early physiological changes observed in fish after exposure to Chattonella spp. (Ishimatsu et al, 1990(Ishimatsu et al, , 1991Tsuchiyama et al, 1992). Yellowtail were exposed to two strains of C. marina that had been subjected to differing light-dark regimes, filtering, mechanical disruption, freezing, or disturbance by mechanical agitation; the highest fish mortality (19 out of of 20) occurred in the presence of intact cells.…”

Histological Analysis of the Mechanisms of <i>Chattonella</i>-Induced Hypoxemia in Yellowtail

“…However , these alterations were hardly detectable at the time of Pao2 drop and therefore cannot be the cause of hypoxemia . Ishimatsu et al7,8) found other physiological perturbations , such as acidosis and an elevation of plasma ions , becoming manifest toward the death. These may be related to destruction of the ion transport capacity caused by chloride cell dysfun ctioning.…”

Antioxidant responses and lipid peroxidation in gills and erythrocytes of fish (Rhabdosarga sarba) upon exposure to Chattonella marina and hydrogen peroxide: Implications on the cause of fish kills

“…Several hypotheses have been proposed, including gill damage and hence impairment of oxygen transfer (Matsusato & Kobayashi, 1974;Sakai et al, 1986;Endo et al, 1988;Ishimatsu et al, 1990Ishimatsu et al, , 1991Ishimatsu et al, , 1996aIshimatsu et al, , 1996bTsuchiyama et al, 1992;Oda et al, 1995Oda et al, , 1997Oda et al, , 1998, production of neurotoxins (Onoue & Nozawa, 1989;Endo et al, 1992;Khan et al, 1996 b; and polyunsaturated fatty acids (PUFAs) (Nichols et al, 1987;Suzuki & Matsuyama, 1995), as well as generation of reactive oxygen species (ROS) by Chattonella spp. (Shimada et al, 1991(Shimada et al, , 1993Oda et al, 1992aOda et al, , 1992bOda et al, , 1994Oda et al, , 1995Oda et al, , 1997Kim et al, 1999a).…”