"Activation" of alveolar leukocytes isolated from cats fed taurine-free diets.
Taurine is a ubiquitous amino sulfonic acid in mammals, present in high concentrations in tissues, including those exposed to elevated levels of oxidants. Experiments were designed to examine the consequences of taurine deficiency on production of ROI in leukocytes isolated from the lungs and blood of cats fed taurine-deficient diets. Cats were maintained on taurine-free or taurine-supplemented diets for at least 12 months at which time taurine deficiency was evident. To analyze alveolar cells, lungs were lavaged to recover lung macrophages and PMNs. Lung lavage fluid from cats contained macrophages and PMNs, although taurine deficiency was associated with a decrease in the percentage of PMNs in the lungs. This is similar to our findings in blood that taurine deficiency reduced the proportion of PMNs. Taurine measurements revealed 2.1 +/- 1.6 mumol/g wet wt of taurine in the lungs from cats fed a taurine-deficient diet versus 8.3 +/- 2.6 in lungs from cats fed a diet supplemented with taurine (n = 16). The effects of taurine deficiency on the functional activity of lung macrophages and PMNs were analyzed including the production of ROI. Alveolar leukocytes from cats fed taurine-deficient diets produced more superoxide anion in response to phorbol myristate acetate than cats fed taurine supplemented diets. Similar results were obtained using a chemiluminescence assay. Using the highly specific H2O2 indicator dye, dichlorofluorescin, and flow cytometry we found that alveolar leukocytes made more H2O2 than cells from cats fed taurine-supplemented diets. Forty-two percent of the cells from cats fed a taurine-supplemented diet expressed class II antigens. In contrast, 72% of cells from the taurine-deficient cats expressed this antigen. We hypothesize that taurine functions to prevent terminal activation and release of cytotoxic mediators by lung macrophages. Thus, a deficiency of taurine will indeed cause an activation of leukocytes, as evidenced by our data which show an increase in ROI, as well as an increase in class II antigen.
Schuller-Levis
G B
GB
New York State Institute for Basic Research in Developmental Disabilities, Staten Island 10314.
Sturman
J A
JA
D000596:Amino Acids / Q000032:analysis; D000818:Animals; D000954:Antigens, Surface / Q000032:analysis; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D002415:Cats / Q000378:metabolism / Q000502:physiology*; D004032:Diet; D005260:Female; D005434:Flow Cytometry; D005453:Fluorescence; D066298:In Vitro Techniques; D008262:Macrophage Activation / Q000502:physiology*; D016676:Macrophages, Alveolar / Q000502:physiology*; D009504:Neutrophils / Q000502:physiology*; D016897:Respiratory Burst / Q000502:physiology; D013481:Superoxides / Q000032:analysis; D013654:Taurine / Q000172:deficiency*
D000596:Amino Acids; D000954:Antigens, Surface; D013481:Superoxides; D013654:Taurine