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The present study was performed to elucidate the mechanisms responsible for the changes of melanin content/ distribution we had previously discovered in the liver parenchyma of Rana esculenta during natural hibernation.Melanomacrophagic component response was analysed using morphocytochemical methods. The results demonstrated that during the prehibernation period (October-November) the melanomacrophages reach the highest proliferative activity (BrdU, PCNA labelling) which is accompanied by an evident melanosynthesis (dopa-oxidase activity). In contrast, after hibernation, the decrease of liver pigmentation was the consequence of a partial cell loss by apoptotic mechanisms (TUNEL labelling, pyknosis-karyorhexis) accompanied by a decrease of melanosome content by autophagy and low melanosynthetic activity. On the basis of these findings, there is evidence that liver

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. Composition, biophysical properties, and morphometry of plasma membranes in pulmonary interstitial edema. Am J Physiol Lung Cell Mol Physiol 282: L1382-L1390, 2002. First published February 1, 2002 10.1152/ajplung.00447.2001.-We evaluated the changes in plasma membrane composition, biophysical properties, and morphology of pulmonary endothelial cells in anesthetized rabbits receiving 0.5 ml ⅐ kg Ϫ1 ⅐ min Ϫ1 saline infusion for 180 min, causing mild interstitial edema. Plasma membrane fractions were obtained from lung homogenates with gradient centrifugation, allowing a sixfold enrichment in caveolin-1. In edematous lungs, cholesterol content and phospholipidic phosphorus increased by 15 and 40%, respectively. These data correlated with morphometric analysis of lungs fixed in situ by vascular perfusion with 2.5% glutaraldehyde, suggesting a relative increase in surface of luminal to interstitial front of the capillary endothelial cells, due to a convoluted luminal profile. In edematous lungs, the fraction of double-bound fatty acids increased in membrane lipids; moreover, the phosphatidylcholine/phosphatidylethanolamine and the cholesterol/phospholipid ratios decreased. These changes were consistent with the increase in fluorescence anisotropy of plasma membrane, indicating an increase in its fluidity. Data suggest that mechanical stimuli elicited by a modest (ϳ4%) increase in extravascular water cause marked changes in plasma membranes that may be of relevance in signal transduction and endothelial cell activation. rabbit; air-blood barrier; endothelial cells; membrane composition and fluidity THE ALVEOLAR AND CAPILLARY walls delimit the pulmonary interstitium, a thin compartment made of a fiber system, serving as a scaffold, and other macromolecules forming the capillary and the alveolar basement membranes. Extravascular water is distributed within the interstitial compartment of the air-blood barrier and is physiologically kept at a minimum volume to optimize gas diffusion. Recent work, based on an experimental model causing a mild form of pulmonary interstitial edema, allowed us to describe the mechanisms contributing to a tight control of extravascular lung volume in the air-blood barrier (6,20). These studies also showed that, despite a remarkable resistance of the pulmonary tissue to edema formation, the increase in interstitial fluid volume occurs as a consequence of fragmentation of proteoglycans, important macromolecules of the extracellular matrix (24,25,31,32) controlling microvascular permeability and tissue mechanical resistance. We wished to further investigate the condition of mild interstitial edema because it represents a critical equilibrium between matrix degradation and deposition provided by cellular activation. We focused on cellular involvement in mild interstitial edema, particularly on the composition and fluidity of plasma membranes that are known to be sensitive to alterations in chemical and physical stimuli of the environment surrounding the cells (34, 36). MATERIALS AND METHODS C...

Reactive oxygen species (ROS) and nitric oxide (NO) have a role in the development of pulmonary fibrosis after bleomycin administration. The ROS production induces an antioxidant response, involving superoxide dismutases (SODs), catalase, and glutathione peroxidases. We compared in situ oxidative burden and antioxidant enzyme activity in bleomycin-injured rat lungs and normal controls. ROS expression and catalase, glucose-6-phosphate-dehydrogenase (G6PHD), and NOS/NADPH-diaphorase activity were investigated by using histochemical reactions. Nitric oxide synthase (e-NOS and i-NOS) and SOD (MnSOD, Cu/ZnSOD, ECSOD) expression was investigated immunohistochemically. After treatment ROS production was enhanced in both phagocytes and in type II alveolar epithelial cells. Mn, Cu/Zn, and ECSOD were overexpressed in parenchymal cells, whereas interstitium expressed ECSOD. Catalase and G6PHD activity was moderately increased in parenchymal and inflammatory cells. NOS/NADPH-d activity and i-NOS expression increased in alveolar and bronchiolar epithelia and in inflammatory cells. It can be suggested that the concomitant activation of antioxidant enzymes is not adequate to scavenge the oxidant burden induced by bleomycin lung damage. Inflammatory cells and also epithelial cells are responsible of ROS and NO production. This oxidative and nitrosative stress may be a substantial trigger in TGF-beta1 overexpression by activated type II pneumocytes, leading to fibrotic lesions.