To determine the effects of dietary fat saturation on plasma lipoproteins, we studied 21 free-living normolipidemic women (13 pre- and 8 postmenopausal) on three consecutive diet periods. During the first 4 wk they consumed a saturated diet rich in palm oil and butter [19% saturated fatty acids (S), 14% monounsaturated fatty acids (M), and 3.5% polyunsaturated fatty acids (P)], followed by 6 wk of a monounsaturated diet rich in olive oil (11% S, 22% M, and 3.6% P), and 6 wk of a polyunsaturated diet rich in sunflower oil (10.7% S, 12.5% M, and 12.8% P). Compared with the diet rich in saturated fatty acids, both diets rich in unsaturated fatty acids had similar lowering effects on total and low-density-lipoprotein cholesterol. High-density lipoprotein cholesterol and apolipoprotein A-I were higher in the monounsaturated-rich period than in the polyunsaturated-rich (10.5% and 12.7% respectively, P less than 0.001) and the saturated-rich period (5.3%, and 7.9%, respectively, P less than 0.05). These effects were independent of menopause status. Our data show that at this level of fat intake (36% as calories), a monounsaturated-rich diet results in a less atherogenic lipid profile than either polyunsaturated- or saturated-rich diets.

The effect of dietary-fat saturation on plasma lipoprotein concentrations was assessed in 46 men and 32 women placed on a diet enriched in polyunsaturated fatty acids (sunflower oil) for 12 wk and, under isocaloric conditions, on a diet enriched in monounsaturated fatty acids (olive oil) for the next 16 wk in men and 28 wk in women. Fat comprised 37% of the total energy intake in men and 36% in women. At the end of the monounsaturated fatty acid diet no change occurred in total cholesterol (TC) in men but it increased by 9% in women. High-density-lipoprotein (HDL) cholesterol increased by 17% in men and by 30% in women. The atherogenic index (TC:HDL cholesterol) fell significantly in both sexes. No significant changes occurred in plasma low-density-lipoprotein cholesterol or in total triglycerides values. These data show that when compared with polyunsaturates, monounsaturates increased HDL cholesterol and reduced the atherogenic risk profile in both sexes.

This study investigated the effect of cigarette smoke exposure and the potential protection N-acetylcysteine (NAC) in rat lungs.Forty-eight rats were exposed to cigarette smoke (CS) for 10 weeks, without (CS group) or with (CS+NAC group) oral intake of NAC 200 mg . rat -1 . day -1 , or to fresh air (Control). All rat lungs were assessed in terms of lung function, ventilation distribution (nitrogen, helium and sulphur hexafluoride phase III slopes), and morphometry (airway wall thickening of small, medium and large bronchi).The small bronchi, defined as the airways with an internal perimeter <1,000 mm showed significantly thicker airway walls in the CS than in the Control group. By contrast, no airway wall thickening was observed in the CS+NAC group with respect to Control. Except for decreased lung volumes and compliance in CS and CS+NAC groups, which were entirely attributable to smaller body weight gain, lung function was indistinguishable from Control. Phase III slopes were significantly increased only in the CS group.In conclusion, smoke-induced alterations in the rat lungs were reflected in wall thickening of the small bronchi and increased ventilation maldistribution. These smoke-induced morphometric and ventilation distribution alterations were prevented by N-acetylcysteine. Eur Respir J 2000; 15: 505±511. In humans, a major site of inflammatory action of cigarette smoke has been attributed to the so-called small airways, stimulating a number of studies aimed at characterizing and detecting structural change in the lung periphery [1,2]. The phase III slope of the N 2 single breath washout (SBW) test became a popular index of small airways alteration since the work by COSIO et al. [3] showed its correlation with morphological scores of small airways abnormalities in smokers with normal spirometry. A later SBW study by VAN MUYLEM et al. [4], which included helium and sulphur hexafluoride tracer concentrations, also revealed distinct correlations between indices derived from He and SF 6 slopes and airway pathology scores. Due to the fact that the diffusion front is located more peripherally for SF 6 than for He, the respective phase III slopes are indicative of the site where ventilation inhomogeneities occur.Although animal studies are well-suited for the study of lung function in the diseased lung, the difficulty often resides in reproducing a lesion which is comparable to that encountered in the human lung [5]. Previous studies in rats have led to conflicting results as to whether the cigarette smoke induces emphysematous lesions [6,7] or not [8,9] and not all studies provide any information about the extent to which the nonalveolated airways are affected [10]. Despite these difficulties, rat lungs have been used to investigate the possible protective role of N-acetylcysteine (NAC) over cigarette smoke induced lesions. NAC is an antioxidant and can therefore be expected to change lung oxidant-antioxidant imbalance induced by cigarette smoke which is a source of oxidants. Previous histopathology...

1. The aim of the present study was to perform an evolutionary analysis of the morphometrical, biochemical and functional parameters of centriacinar emphysema induced by cadmium chloride (CdCl2) in rats and to determine the effects of concomitant N-acetylcysteine (NAC) administration. 2. Male Wistar rats were instilled orotracheally with either CdCl2 (n = 24) or saline (n = 24). One group of rats, consisting of both CdCl2- and saline-treated rats, was fed a normal diet (n = 24), whereas the other group received NAC (n = 24). 3. Changes in inspiratory capacity (IC), lung compliance (CL), expiratory flow at 75% (F75), forced vital capacity (FVC) and hydroxyproline content were assessed 2, 8, 21 and 45 days after instillation. Polymorphonuclear cells were evaluated 2 and 8 days after instillation and the mean linear intercept (Lm) was determined at 21 and 45 days. 4. Over time, CdCl2 instillation causes several changes that are bound up with centriacinar emphysema. The concomitant administration of NAC to CdCl2-treated rats partially reversed Lm at 21 days compared with CdCl2 alone (115 +/- 2 vs 127 +/- 2, respectively; P < 0.05). However, 45 days after instillation, NAC improved lung function in CdCl2-treated rats compared with that in the saline-treated control group (IC 14.64 vs 15.25, respectively (P = 0.054); FVC 16.94 vs 16.28, respectively (P = 0.052), F75 31.41 vs 32.48, respectively (P = 0.062)). In addition, 45 days after instillation, NAC reduced lung collagen content in both the saline-treated control (100 vs 81% alone and in the presence of NAC, respectively) and CdCL2-treated groups (213 vs 161% alone and in the presence of NAC, respectively). In addition, although the results were not significant, NAC tended to reduce Lm and enhance CL in NAC + CdCl2-treated rats. 5. In conclusion, NAC partially improved emphysematous changes and reduced collagen deposition, which diminished the CdCl2-induced fibrotic component of centriacinar emphysema.