We investigated the consequences of feeding for acid-base balance, nitrogen excretion, blood metabolites and osmoregulation in the Pacific spiny dogfish. Sharks that had been starved for 7·days were surgically fitted with indwelling stomach tubes for gastric feeding and blood catheters for repetitive blood sampling and were confined in chambers, allowing measurement of ammonia-N and urea-N fluxes. The experimental meal infused via the stomach tube consisted of flatfish muscle (2% of body mass) suspended in saline (4% of body mass total volume). Control animals received only saline (4% of body mass). Feeding resulted in a marked rise in both arterial and venous pH and HCO 3 -concentrations at 3-9·h after the meal, with attenuation by 17·h. Venous P O ∑ also fell. As there were negligible changes in P CO ∑, the response was interpreted as an alkaline tide without respiratory compensation, associated with elevated gastric acid secretion. Urea-N excretion, which comprised >90% of the total, was unaffected, while ammonia-N excretion was very slightly elevated, amounting to <3% of the total-N in the meal over 45·h. Plasma ammonia-N rose slightly. Plasma urea-N, TMAO-N and glucose concentrations remained unchanged, while free amino acid and β-hydroxybutyrate levels exhibited modest declines. Plasma osmolality was persistently elevated after the meal relative to controls, partially explained by a significant rise in plasma Cl -. This marked post-prandial conservation of nitrogen is interpreted as reflecting the needs for urea synthesis for osmoregulation and protein growth in animals that are severely N-limited due to their sporadic and opportunistic feeding lifestyle in nature.

The Amazonian oscar is extremely resistant to hypoxia, and tolerance scales with size. Overall, ionoregulatory responses of small (ϳ15 g) and large oscars (ϳ200 g) to hypoxia were qualitatively similar, but the latter were more effective. Large oscars exhibited a rapid reduction in unidirectional Na ϩ uptake rate at the gills during acute hypoxia (PO2 ϳ10 mmHg), which intensified with time (7 or 8 h); Na ϩ efflux rates were also reduced, so net balance was little affected. The inhibitions were virtually immediate (1st h) and preceded a later 60% reduction (at 3 h) in gill Na ϩ -K ϩ -ATPase activity, reflected in a 60% reduction in maximum Na ϩ uptake capacity without change in affinity (Km) for Na ϩ . Upon acute restoration of normoxia, recovery of Na ϩ uptake was delayed for 1 h. These data suggest that dual mechanisms may be involved (e.g., immediate effects of O 2 availability on transporters, channels, or permeability, slower effects of Na ϩ -K ϩ -ATPase regulation). Ammonia excretion appeared to be linked indirectly to Na ϩ uptake, exhibiting a Michaelis-Menten relationship with external [Na ϩ ], but the Km was less than for Na ϩ uptake. During hypoxia, ammonia excretion fell in a similar manner to Na ϩ fluxes, with a delayed recovery upon normoxia restoration, but the relationship with [Na ϩ ] was blocked. Reductions in ammonia excretion were greater than in urea excretion. Plasma ammonia rose moderately over 3 h hypoxia, suggesting that inhibition of excretion was greater than inhibition of ammonia production. Overall, the oscar maintains excellent homeostasis of ionoregulation and N-balance during severe hypoxia. teleost fish; ionoregulation; nitrogen metabolism; sodium-potassiumATPase; ion channels THE PRESENT STUDY USES the hypoxia-tolerant oscar (acará-açu; Astronotus ocellatus), an entirely water-breathing Amazonian cichlid, to examine the effects of low environmental O 2 on two key aspects of gill function, ionoregulation and nitrogenous waste excretion. The oscar commonly encounters hypoxia in its natural environment when it enters the seasonally flooded jungle to feed and reproduce; adults are reported to survive up to 6 h of complete anoxia and can tolerate levels of 5-20% air saturation for 20 -50 h (1, 2, 32). There are several reasons for believing that ionic balance and ammonia excretion may be particularly sensitive to hypoxia in freshwater fish, but to date, these areas have received little experimental attention.First, the respiratory-osmoregulatory compromise at the gills has been well documented in exercise studies on several teleost species: the effective gill area and diffusion distance are adjusted as a trade-off between providing the permeability required for gas exchange, while minimizing diffusive ion losses and osmotic water gain (12, 13, 57, 58). During environmental hypoxia, it is probable that similar lamellar recruitment and decreased diffusion distance occurs to help sustain O 2 uptake (17, 18) because gill O 2 transfer factor, an index of effective O 2 permeability, increase...

SUMMARY The physiological and behavioural responses of two size groups of oscar(Astronotus ocellatus) to hypoxia were studied. The physiological responses were tested by measuring ṀO2 during decreasing environmental oxygen tensions. Larger oscars were better able to maintain oxygen consumption during a decrease in PO2, regulating routine ṀO2 to a significantly lower PO2 threshold (50 mmHg)than smaller oscars (70 mmHg). Previous studies have also demonstrated a longer survival time of large oscars exposed to extreme hypoxia, coupled with a greater anaerobic enzymatic capability. Large oscars began aquatic surface respiration (ASR) at the oxygen tension at which the first significant decrease in ṀO2was seen (50 mmHg). Interestingly, smaller oscars postponed ASR to around 22 mmHg, well beyond the PO2 at which they switched from oxyregulation to oxyconformation. Additionally, when given the choice between an hypoxic environment containing aquatic macrophyte shelter and an open normoxic environment, small fish showed a greater preference for the hypoxic environment. Thus shelter from predators appears particularly important for juveniles, who may accept a greater physiological compromise in exchange for safety. In response to hypoxia without available shelter, larger fish reduced their level of activity (with the exception of aggressive encounters) to aid metabolic suppression whereas smaller oscars increased their activity, with the potential benefit of finding oxygen-rich areas.

Carnitine palmitoyltransferase (CPT) I is regulated by several genetic and non-genetic factors including allosteric inhibition, mitochondrial membrane composition and/or fluidity and transcriptional regulation of enzyme content. To determine the intrinsic differences in these regulating factors that may result in differences between tissues in fatty acid oxidation ability, mitochondria were isolated from red, white and heart muscles and liver tissue from rainbow trout. Maximal activity (V(max)) for beta-oxidation enzymes and citrate synthase per mg tissue protein as well as CPT I in isolated mitochondria followed a pattern across tissues of red muscle>heart>white muscle>liver suggesting both quantitative and qualitative differences in mitochondria. CPT I inhibition showed a similar pattern with the highest malonyl-CoA concentration to inhibit activity by 50% (IC(50)) found in red muscle while liver had the lowest. Tissue malonyl-CoA content was highest in white muscle with no differences between the other tissues. Interestingly, the gene expression profiles did not follow the same pattern as the tissue enzyme activity. CPT I mRNA expression was greatest in heart>red muscle>white muscle>liver. In contrast, PPARalpha mRNA was greatest in the liver>red muscle>heart>white muscle. There were no significant differences in the mRNA expression of PPARbeta between tissues. As well, no significant differences were found in the mitochondrial membrane composition between tissues, however, there was a tendency for red muscle to exhibit higher proportions of PUFAs as well as a decreased PC:PE ratio, both of which would indicate increased membrane fluidity. In fact, there were significant correlations between IC(50) of CPT I for malonyl-CoA and indicators of membrane fluidity across tissues. This supports the notion that sensitivity of CPT I to its allosteric regulator could be modulated by changes in mitochondrial membrane composition and/or fluidity.