Dietary beta-carotene protects lung and liver parenchyma of rats treated with monocrotaline.

Some studies have indicated that the injury induced by the hepato- and pneumotoxin monocrotaline (MCT) is in part mediated by oxidation. Because beta-carotene is a potent antioxidant, we hypothesized that it would protect the lung and liver parenchyma against MCT-induced injury. Twenty rats were assigned randomly to four groups. All rats were fed a standard AIN93G diet with or without beta-carotene. After 1 week on the purified diets, half of the rats fed the control (standard) diet and half of the rats fed the beta-carotene-supplemented diet were injected subcutaneously with 60 mg MCT/kg body weight or its vehicle (water). All rats were sacrificed at 4 weeks. Histological examination showed that beta-carotene alone did not affect lung or liver structure. On the other hand, lungs of MCT-treated rats had severe focal pneumonia, extensive deposition of collagen in the septa, marked inflammation of the small arteries and arterioles, and arterialization of the small venules. Livers of MCT-treated rats showed some fatty infiltration and diffuse hemorrhages, more prominent sometimes in the centrilobular area and sometimes in the periportal region. Concomitant treatment with beta-carotene protected the lung parenchyma from the inflammatory reaction and the septal fibrosis, but did not prevent cardiac right ventricular hypertrophy and only slightly reduced the thickening of the wall of small arteries and arterioles. Incidence of steatosis and hemorrhages was decreased in the liver. These results indicate that MCT-induced pulmonary vascular remodeling occurs in the absence of inflammatory cell infiltration. Furthermore, beta-carotene prevented inflammation and protected the lung and liver parenchyma of MCT-treated rats.

Dietary retinol inhibits inflammatory responses of rats treated with monocrotaline.

This study was designed to test the effectiveness of dietary retinol in protecting the heart and lung parenchyma in a monocrotaline model for lung injury and pulmonary hypertension in rats. Male rats were assigned to three groups. Two groups were injected subcutaneously with monocrotaline (17 mg/kg body weight) and fed either the control AIN-93G diet (MC) or the control diet supplemented with retinol (17 mg retinyl palmitate/kg diet)(MR). The third group was fed the control diet and injected with the vehicle only (VC). Four weeks after monocrotaline treatment, the MR group had less thickening of the alveolar septal wall, less myocardial inflammation and degeneration of the right ventricle, and less vascular inflammation in the lung compared with the MC group. The supplemented dietary retinol, however, did not prevent development of right ventricular hypertrophy and did not affect the synthesis and secretion of surfactant phospholipids in type II pneumocytes. The results indicate that dietary retinol suppresses the inflammatory responses in the heart and lungs of rats treated with monocrotaline.

The effects of dietary fish oil on alveolar type II cell fatty acids and lung surfactant phospholipids.

The purpose of this study was to determine the responsiveness of alveolar type II cells to dietary fish oil and the consequent effects on alveolar and lung surfactant. Rats were fed a corn oil or a fish oil diet for four weeks. Dietary n-3 fatty acids were readily incorporated into the type II cell phospholipids as indicated by higher levels of eicosapentaenoic acid (2.77 +/- 0.10%) and docosahexaenoic acid (1.63 +/- 0.10%) in the group receiving the fish oil diet. The elevated levels of n-3 fatty acids were accompanied by concomitant reduction in arachidonic acid and linoleic acid. Neither eicosapentaenoic acid nor docosahexaenoic acid was incorporated into type II cell triacylglycerols. Feeding a fish oil containing diet increased surfactant phospholipids, particularly 1,2-disaturated acyl phosphatidylcholines in whole lung compared to a corn oil diet. However, the amount of surfactant found in the alveolus was not different between the two diet treatment groups. The results suggest that dietary n-3 fatty acids stimulate synthesis and/or inhibit degradation of lung surfactant without altering surfactant secretion in alveoli.