The effects of pyrene exposure on exercise performance, muscle contraction, and mitochondrial O(2) consumption in the leopard frog (Rana pipiens).

The present study exposed frogs to the PAH pyrene and measured exercise performance, muscle contractile ability, mitochondrial O(2) consumption, and membrane potential. Leopard frogs, Rana pipiens, were exposed for seven days in control or pyrene saturated water aquaria. Frogs were randomly placed into one of four groups: (i) pyrene-exposed exercised, (ii) control, exercised, (iii) pyrene-exposed, non-exercised, and (iv) control, non-exercised. Following the acute exposure, exercise duration, muscle contractile ability, blood gases and pH, glycogen levels, crossbridge formation and contractile length, and mitochondrial respiration were measured. The data revealed that pyrene exposure produced many adverse effects in Leopard frogs including significant reductions in exercise performance, muscle contractile ability, and alterations to muscle mitochondrial O(2) consumption and membrane potential. These data suggest that PAH exposure may limit survival for frogs in the wild by limiting foraging, mating, and predator avoidance behaviors.

Uptake and elimination of naphthalene from liver, lung, and muscle tissue in the leopard frog (Rana pipiens).

The effects of a 0-12-hour naphthalene exposure on pulmonary CO(2) excretion and bioaccumulation in the leopard frog, Rana pipiens, were investigated. The data showed that naphthalene transport occurred from the aqueous phase into the frog tissue. The first-order rate constant (k in day-1) for the entry of naphthalene from the water into the frog was 0.079 +/- 0.007 (k +/- 95% C.I.). Bioaccumulation of naphthalene was measured in liver, lung, and thigh muscle tissue. Exposure to naphthalene caused a significant reduction in pulmonary CO(2) excretion, particularly following the first 30 minutes of exposure. Pulmonary CO(2) excretion returned to baseline levels after 8 hours of exposure, indicating that some degree of acclimation had occurred. Depuration experiments were used to monitor recovery from naphthalene exposure. Recovery of CO(2) excretion was evident following 2 hours of depuration and complete elimination of naphthalene from tissues occurred after 3 hours. The data indicate that accumulated polycyclic aromatic hydrocarbons (PAHs) may alter normal physiologic functions such as gas exchange. Since amphibians, such as frogs, are one of the first organisms to come into contact with contaminated water and sediments, the information in this study suggests that this species may be used to assess bioaccumulation and toxicity of PAHs in ecosystems.

Pulmonary carbonic anhydrase in vertebrate gas exchange organs.

Carbonic anhydrase (CA) catalyzes the interconversion of CO(2) and HCO(3)(-). Intracellular (extravascular) and intravascular (extracellular) CA has been identified and localized in the lungs of reptiles and mammals. Less information is known, however, on the presence of intravascular CA in the lungs of amphibians and avians. In the present study, perfusion studies were used to compare the catalytic activity of pulmonary intravascular CA in reptiles and mammals. In addition, SDS-resistant CA activity was examined in microsomal fractions prepared from gill/lung tissue from representative animals in each vertebrate class. Finally, the CNO(-) sensitivity of the microsomal CA activity was compared. No SDS-resistant CA activity was found in gill microsomal fractions of several fish species. In contrast, the data suggest that SDS-resistant, intravascular pulmonary CA activity is present in air-breathing vertebrates with vastly differing lung morphologies and that the kinetics of inhibition is remarkably comparable between the vertebrate classes.

Pulmonary carbonic anhydrase in the garter snake, Thamnophis sirtalis.

This study examined whether the snake lung possesses intravascular carbonic anhydrase (CA). Lungs were perfused with control salines and with salines containing CA inhibitors. Perfusion with control salines resulted in a stable CO(2) excretion, whereas CA inhibitors significantly reduced pulmonary CO(2) excretion. Membrane-permeable and membrane-impermeable CA inhibitors produced comparable decreases in CO(2) excretion, suggesting that extracellular, intravascular CA participated in the pulmonary CO(2)-HCO3(-)-H(+) reactions. Treatment of lungs with phosphatidylinositol specific-phospholipase C (PI-PLC) significantly decreased CO(2) excretion, indicating that CA was connected to the luminal endothelial cell membrane by a phosphatidylinositol glycan linkage. Taken together, these results are the first to demonstrate the presence of membrane-bound, intravascular CA (CA IV) in the snake lung.