Effects of orally administered insecticides and polychlorinated biphenyls on the parasite fauna of two species of piscivorous birds

A study was initiated to determine the effects of various levels of ingested DDT and its metabolites and polychlorinated biphenyls on young double-crested cormorants, Phalacrocorax a. auritus, and white pelicans, Pelencanus erythrorhynchos. One phase of this research was concerned with the effects of ingested insecticides and polychlorinated biphenyls on the parasite fauna of these birds. Statistical analysis indicated a decrease in the numbers of ectoparasites on the feathers of cormorants as dosage of insecticides and as residue levels on the feathers increased. Similar results were noted with ectoparasites and gular lice of white pelicans receiving a daily dosage of either polychlorinated biphenyls or a mixture of DDT, DDD, and DDE. There were no significant differences in the numbers of endoparasites between the control and treated birds in either the cormorants or pelicans.     

Release and specific binding of prostaglandins in bovine pineal gland

Incubated bovine pineal glands released prostaglandin E- and prostaglandin F-like material (304 ± 20 and 582 ± 56 pg/mg dry tissue wt/h, respectively) and the release was increased 2.2 2.9-fold by adding 10⁻⁴–10⁻⁶M of norepinephrine to the medium. Binding assays revealed the existence of high affinity binding of ³H-prostaglandin E₂ (³H-PGE₂) and ³H-prostaglandin F_2α (³H-PGF_2α) in low speed supernatants of pineal homogenates. Binding was increased by increasing Ca⁺⁺ concentration in medium up to 2 mM, was heat-labile and was depressed following incubation with trypsin. In subcellular fractionation studies maximal ³H-PG binding was found in the 27000 × g pellet. Scatchard analysis of ³H-PGE₂ binding revealed the presence of a single population of binding sites with a K_d= 1.2 nM and a binding site concentration of 1–2 pmoles/g protein. A single population of binding sites for ³H-PGF_2α was also detected with a K_d= 1.7 nM and a similar binding site concentration. Non-radioactive PGE₁ and PGE₂ were almost equally effective to compete for ³H-PGE₂ binding sites (ED₅₀= 5 and 2 nM, respectively). Unlabeled PGF₂ was relatively ineffective to compete for ³H-PGE₂ binding (ED₅₀>1000 nM) but displaced effectively ³H-PGF_2α binding (ED₅₀= 1.2 nM).     

Role of glucose metabolism in acid formation by isolated gastric glands

The role played by glucose in providing energy for acid formation was studied in isolated gastric glands from rabbit. The widely-used inhibitors of glycolysis, iodoacetic acid and iodoacetamide were found to inhibit glucose oxidation as well as the indicators of acid formation, respiration and accumulation of aminopyrine. However, the potent inhibition of acid formation was found to involve a nonspecific mechanism other than the simple inhibition of glycolysis. An alternative approach involved use of the glucose transport inhibitor, phloretin. Phloretin blocked glucose oxidation and also inhibited functional responses. Acid formation was restored easily by the addition of pyruvate or various other oxidizable substrates. Measurement of lactate formation in the absence of exogenous glucose showed that the gastric glands contain very little glycogen. Addition of external glucose resulted in a 10-fold increase in lactate formation and this rate was stimulated further by histamine and rotenone. Rotenone also inhibited both respiration and aminopyrine accumulation; however, the inhibition was not complete. Phloretin treatment resulted in total inhibition of the residual aminopyrine accumulation after rotenone treatment. The results are interpreted to indicate that gastric glands are dependent almost totally on external substrate supply to support acid formation; and, that while anaerobic glucose metabolism can sustain a very low level of acid formation, the major role of glucose is to yield pyruvate equivalents for subsequent oxidation.