Suppressive Effect of β-Carotene on the Development of Pulmonary Foam Cells in Rats with Hyper β-Lipoproteinemia

Shibuya, Kazumoto; Tajima, Masanori; Saitoh, Toshiki; Yamate, Jyoji; Nunoya, Tetsuo

doi:10.1177/019262339502300106

Cited by 3 publications

(5 citation statements)

References 23 publications

(13 reference statements)

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“…In these rats, the parallel increase in numbers of FMs in the blood and PFCs in the lungs was observed, coinciding with our previous findings (15,17). Most of AMs have been shown to derive directly from BMs, while a small proportion was produced by division of resident interstitial macrophages (2,3).…”

Section: Phagocytotic Activity Of Bmssupporting

confidence: 92%

“…One or 2 rats were housed in each wire-mesh cage, and the animals were maintained in a barrier-sustained room controlled at 23 ± 2°C and 50 ± 20% relative humidity, with a 12-hr light-dark cycle. The rats were allocated to 4 groups: rats in the control group were given a standard commercial diet for rats (NR-2, Laboratory Animal Research Station, Yamanashi, Japan); rats in the HB group were fed the HB diet consisting of NR-2, 4% cholesterol, and 1 % cholic acid; rats in the CCI,-administered (CT) group received NR-2 and were administered ip with 1.0 ml/kg of CC'4 fortnightly; rats in the HT group received the HB diet and were ad- (15).…”

Section: Methodsmentioning

confidence: 99%

“…Mononuclear leukocytes were separated from a portion of the blood that was collected from 4 rats of each group by the method described (15). Alveolar macrophages (AMs) were collected from the right and accessory lung lobes by the method described by Phizackerley et al (11 (Fig.…”

Section: Methodsmentioning

confidence: 99%

“…Most of AMs have been shown to derive directly from BMs, while a small proportion was produced by division of resident interstitial macrophages (2,3). Our previous experimental studies on rats revealed that hyper r3-lipoproteinemia enhanced the foamy transformation of BMs, emigration of FMs into the pulmonary alveoli, and development of PFCs (17), and it has been surmised that BMs might ingest excess amounts of oxidatively modified B-LP via the receptor pathway because the development of FMs and PFCs was suppressed in HB rats by treatment with r3-carotene, an antioxidant, and no differences in phagocytotic activity of BMs were observed between HB rats with and without the r3-carotene treatment (15 (6). Oxidatively modified LDL particles also underwent aggregation or enlargement (22), and then aggregated particles were avidly phagocytosed by macrophages (6,20).…”

Section: Phagocytotic Activity Of Bmsmentioning

confidence: 99%

“…Our previous studies revealed that foamy transformation of blood monocytes (BMs), emigration of BMs into the pulmonary alveoli, and the development of PFCs were enhanced in rats under the diet-induced hyper (3-lipoproteinemic (HB) condition (17) and that these phenomena were suppressed by treatment with (3-caro-tene, a natural antioxidant (15). These observations suggest that oxidative B-LP may be uptaken actively by BMs, leading to the development of PFCs in rats.…”

Section: Introductionmentioning

confidence: 99%

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Carbon Tetrachloride-Induced Hepatotoxicity Enhances the Development of Pulmonary Foam Cells in Rats Fed a Cholesterol-Cholic Acid Diet

et al. 1997

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The effect of CCl 4 -hepatotoxicity on the development of pulmonary foam cells (PFCs) was studied using 4 groups of rats. Rats in the control group were fed a standard diet; rats in the second group were fed a hyper β-lipoproteinemic (HB) diet consisting of the standard diet, 4% cholesterol, and 1% cholic acid; rats in the third group were fed the standard diet and administered with CCl 4 (1.0 ml/kg, ip, fortnightly) (CT); and rats in the fourth group were fed the HB diet and administered with CCl 4 (HT). At feeding week 10, rats in the HB and HT groups developed hyper β-lipoproteinemia. The ratios of foamy, lipid-ingested monocytes (FMs) to blood monocytes (BMs) and the histologic scores of PFC development were significantly greater in the HB and HT groups than in the control and CT groups, respectively. The ratio of PFCs to alveolar macrophages from bronchopulmonary lavage fluid was significantly higher in the HT group than in the CT group. At feeding week 20, rats in the CT and HT groups suffered hepatic injury and hypo β-lipoproteinemia. Despite hypo β-lipoproteinemia, the FM and PFC development, the ratio of BMs in differential leukocyte counts, and latex-phagocytotic activity of BMs were enhanced in the HT group. Furthermore, markedly enlarged FMs, described here as giant-FMs, that contained numerous lipid droplets in their abundant cytoplasm appeared in the peripheral blood from rats in the HT group. Histologically, embolism caused by giant-FMs in the pulmonary blood vessels and intraalveolar accumulation of PFCs were detected with a high incidence in the HT group. The present study suggests that CCl 4 -hepatotoxicity may affect lipoprotein synthesis in the liver of hyper β-lipoproteinemic rats and defective or modified lipoproteins can be phagocytosed actively by BMs, and then BMs transform into FMs or giant-FMs, resulting in the PFC development and pulmonary embolism by giant-FMs.

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Section: Phagocytotic Activity Of Bmssupporting

confidence: 92%

Section: Methodsmentioning

confidence: 99%