Physiological adaptations of rainbow trout to chronically elevated water pH (pH = 9.5)

Abstract

Recent investigations have demonstrated that rainbow trout cope with acute high pH (pH > 9.0) exposure (lasting 3–8 days) through their ability to counteract high‐pH‐induced disturbances to ammonia excretion (JAmm), acid‐base homeostasis, and electrolyte balance. In the present investigation our goal was to establish how these physiological processes were modulated during chronic (28‐day) high pH (pH = 9.5) exposure. Chronic high pH led to minimal mortality, and there were no long‐term changes in stress indicators levels, such as cortisol or glucose. JAmm was initially reduced by 40% at high pH but rapidly recovered and fluctuated around control rates, thereafter. Decreased JAmm was associated with an initial 2.5‐fold increase in plasma ammonin concentrations (TAmm), followed by a return toward pre‐exposure levels after 3 days. Overall, plasma TAmm was slightly higher (40–80%) in the treatment fish, and this likely led to plasma PNH3s that were sufficient to sustain JAmm at high pH. White muscle TAmm stores were also chronically elevated, by 50–100%. There was a transient, twofold elevation of JUrea immediately following high‐pH exposure, but by 3 days JUrea had returned to control rates and stabilized thereafter. Plasma ion balance was well maintained at high pH, despite a chronic depression of Na+ influx. Even though there was a persistent respiratory alkalosis at alkaline pH, blood pH was effectively regulated by a simultaneous metabolic acid load, which was not associated with increased lactic acid production. White muscle intracellular pH (pHi) was unaltered during high pH exposure. We conclude that the long‐term survival of rainbow trout in alkaline environments is facilitated by higher steady‐state internal ammonia concentrations, the development of a sustained, compensatory metabolic acidosis which offsets decreased plasma PCO2, and the effective regulation of plasma electrolyte balance. © 1996 Wiley‐Liss, Inc.

The effects of strain and ploidy on the physiological responses of rainbow trout (Oncorhynchus mykiss) to pH9.5 exposure

“…The present data shows a significant decrease in plasma chloride at 24 h. The subsequent removal of HCO 3 − via the Cl − / HCO 3 − exchanger at the gills may account for the recovery of chloride by 72 h. This is speculative, as we did not measure plasma HCO 3 − ; however soft water high pH studies have shown increases in HCO 3 − as a result of high pH exposure (Heming and Blumhagen, 1988;Yesaki and Iwama, 1992;McGeer and Eddy, 1998). We expected sodium levels to drop as reported in other trout studies (Wilkie et al, 1993(Wilkie et al, , 1996Wilkie and Wood, 1995), but there were no obvious decreases in plasma sodium much like the study by Wilkie et al (1999). The addition of a total of 0.01 M sodium from NaOH may have assisted in maintaining plasma sodium values.…”

“…Disturbances in ionoregulation occur primarily because high pH causes gill damage by hypertrophy of mucous secreting cells and the degradation of connective tissue between epithelial cells (Daye and Garside, 1976). High pH studies have demonstrated an increase in ion efflux across the gill in freshwater (Wilkie and Wood, 1994;Wilkie et al, 1996), which when coupled with a direct inhibition of ion influx (Wilkie et al, 1999), results in a loss of ions from the plasma.…”

“…The limited change in plasma sodium and chloride suggests that osmoregulation was generally maintained in the trout strains during exposure to pH 9.5. Our results indicate a significant increase in lactate initially, followed by a return to control values by 72 h. This transient increase in plasma lactate is similar to that reported in other studies (Wilkie and Wood, 1991;Wilkie et al, 1996;Wilson et al, 1998), which suggests that pH 9.5 exposure may directly affect aerobic metabolism. Indeed, in mammalian studies, NH 4 Cl addition has been shown to decrease activity of the α-ketoglutarate dehydrogenase complex in the brain (Lai and Cooper, 1986), and decrease pyruvate oxidation in the liver (Maddaiah and Kumbar, 1994), providing mechanisms where aerobic metabolism could be inhibited by the ammonia accumulation resulting from a high pH exposure.…”

“…Whole blood was drawn into heparinized capillary (Ammonium-heparin) tubes after caudal severance. The use of ammonium heparin capillary tubes may have influenced our results; however both control and pH 9.5 exposed fish blood samples were treated identically, and the values we present here are within published values for this species Wood, 1991, 1995;Wilson et al, 1994Wilson et al, , 1998Wilkie et al, 1996;McGeer and Eddy, 1998;Nawata et al, 2007;Sanderson et al, 2010;Zimmer et al, 2014). Capillary tubes were centrifuged at 9200 g to separate plasma from red blood cells and plasma was removed, placed in a microcentrifuge tube, frozen in liquid nitrogen, and stored at −80°C.…”

Observations of Eurasian perch (Perca fluviatilis L.) post-larvae growth performances reared in an illuminated floating cage in Varese lake (N-W Italy) over a two years period

“…In an enclosure experiment, perch survived at pH 10.0 but died when water pH reach a value of 11.0 (Beklioglu and Moss, 1995), suggesting that pH values in Varese lake were often near the upper limit for perch survival. Several laboratory studies have shown that rainbow trout can survive in high pH water for a considerable period of time (15 days at pH 10.0 and 28 days at pH 9.5), due to adjustments to branchial ion movements, acid-base balance, ammonia excretion and production (Wilkie et al, 1996), which may be similar to mechanisms employed by perch in Slapton Lay and Varese lake. In consideration of the trophic state of lake waters, the cage was positioned in the first three meters of water column from the surface, in order to avoid any problem due to anoxic phenomena in the hypolimnion.…”