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Biomedical subjects

A Mezzetti

Publications and source records attributed to A Mezzetti.

At least 55 records · Page 3Linked to original sources

Copper/zinc ratio and systemic oxidant load: effect of aging and aging-related degenerative diseases.

There is evidence that copper and zinc have pro-oxidant and antioxidant properties, respectively, so that their imbalance may be expected to condition oxidative stress status. Oxidative stress is relevant in aging and in age-related degenerative diseases. In this study, blood content of copper, zinc, and ceruloplasmin as well as of lipid peroxides were investigated in 81 healthy and 62 disabled octo-nonagenarians affected by chronic degenerative diseases, and in 81 healthy adults. Serum copper/zinc ratio and ceruloplasmin were significantly higher in the elderly than in the healthy adults. Moreover, all these parameters were significantly higher in the disabled than in the healthy elderly. Notably, the increased copper/zinc ratio found in healthy elderly was due to high copper values, whereas in the disabled, both high copper and low serum zinc concentrations were present. The copper/zinc ratio was significantly and positively related to systemic oxidative stress status in all groups. The higher the serum copper/zinc ratio the higher the lipid peroxides plasma content. We conclude that there is a strict relationship between copper/zinc ratio and systemic oxidant burden. Moreover, advanced age and, particularly, advanced age-related chronic degenerative diseases are associated with a significant increase in the copper/zinc ratio and systemic oxidative stress.

Aged↗

Effect of thyroid function on LDL oxidation.

In this study, the effect of different levels of thyroid hormone and metabolic activity on low density lipoprotein (LDL) oxidation was investigated. Thus, in 16 patients with hyperthyroidism, 16 with hypothyroidism, and 16 age- and sex-matched healthy normolipidemic control subjects, the native LDL content in lipid peroxides, vitamin E, beta-carotene, and lycopene, as well as the susceptibility of these particles to undergo lipid peroxidation, was assessed. Hyperthyroidism was associated with significantly higher lipid peroxidation, as characterized by a higher native LDL content in lipid peroxides, a lower lag phase, and a higher oxidation rate than in the other two groups. This elevated lipid peroxidation was associated with a lower LDL antioxidant concentration. Interestingly, hypothyroid patients showed an intermediate behavior. In fact, in hypothyroidism, LDL oxidation was significantly lower than in hyperthyroidism but higher than in the control group. Hypothyroidism was also characterized by the highest beta-carotene LDL content, whereas vitamin E was significantly lower than in control subjects. In hyperthyroidism but not in the other two groups, LDL oxidation was strongly influenced by free thyroxine blood content. In fact in this group, the native LDL lipid peroxide content and the lag phase were directly and indirectly, respectively, related to free thyroxine blood levels. On the contrary, in hypothyroidism LDL oxidation was strongly and significantly related to serum lipids. In conclusion, both hypothyroidism and hyperthyroidism are characterized by higher levels of LDL oxidation when compared with normolipidemic control subjects. In hyperthyroid patients, the increased lipid peroxidation was strictly related to free thyroxine levels, whereas in hypothyroidism it was strongly influenced by serum lipids.

Antioxidants↗

Low-density lipoprotein oxidation and vitamins E and C in sustained and white-coat hypertension.

Low-density lipoprotein oxidation and antioxidant vitamins E and C were investigated in white-coat hypertension in comparison with sustained hypertension and normotension. We selected 21 sustained hypertensive subjects, 21 white-coat hypertensive subjects, and 21 normotensive subjects matched for gender, age, and body mass index. White-coat hypertension was defined as clinical hypertension and daytime ambulatory blood pressure <139/90 (subjects were also reclassified using 134/90 and 135/85 mm Hg as cutoff points for daytime blood pressure). Blood samples were drawn for lipid profile determination, assessment of fluorescent products of lipid peroxidation in native LDL, evaluation of susceptibility to LDL oxidation in vitro (lag phase and propagation rate), and determination of LDL vitamin E and plasma vitamins E and C contents. Compared with sustained hypertensive subjects, white-coat hypertensives had significantly lower fluorescent products of lipid peroxidation (15.4+/-3.4 versus 10.2+/-3 units of relative fluorescence/mg LDL protein, P<.05), longer lag phase (54+/-10 versus 88+/-10 minutes, P<.05), lower propagation rate (8.2+/-2.5 versus 5.95+/-2.1 nmol diene/min per mg LDL cholesterol, P<.05), higher LDL vitamin E content (8.3+/-1.1 versus 10.1+/-1.8 nmol/mg LDL cholesterol, P<.05), and plasma vitamin C content (40+/-13 versus 57+9 micromol/L, P<. 05). No significant difference was observed between white-coat hypertensive and normotensive subjects. The results did not change after reclassification of subjects. Our data show that white-coat hypertensive subjects do not show an enhanced propensity to LDL oxidation or reduction in antioxidant vitamins. Given the role of LDL oxidation in the development of atherosclerosis and that of vitamin E and C in protecting against it, these findings suggest that white-coat hypertension per se carries a low atherogenic risk.

Adult↗

High-density lipoprotein cholesterol strongly discriminates between healthy free-living and disabled octo-nonagenarians: a cross sectional study. Associazione Medica Sabin.

Aging is frequently associated with a deterioration in health and functional status, which often induces important modifications in several biological parameters, including plasma lipids; as a consequence, the real "meaning" of lipoprotein parameters in old individuals is complex. A cross sectional study was carried out in order to investigate the lipoprotein profile in very old individuals with or without disability, and evaluate the possible influence of other biological variables on plasma lipids. One hundred selected healthy free-living (FL) and 62 disabled (DIS) subjects aged over 80 were enrolled; 91 healthy adults matched for origin were included as controls. Lipoprotein profile [total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol, apoprotein A-I and B], anthropometric parameters, and ADL were measured. The FL octo-nonagenarians featured higher HDL-cholesterol levels than adult controls. DIS octo-nonagenarians showed lower total and HDL-C levels than FL. Discriminant analysis indicated that HDL-cholesterol and apoprotein A-I, but not total cholesterol, strongly discriminated between FL and DIS octo-nonagenarians. Multivariate analysis demonstrated that the waist/hip ratio, an index of visceral adiposity, was negatively associated with HDL-C levels in FL, but not in DIS elderly. We conclude that: 1) in very old individuals, the absence or presence of disability is strongly associated with high or low HDL-cholesterol values, respectively; 2) HDL-C and apo A-I are the parameters which better discriminate between FL and DIS octo-nonagenarians; and 3) the differences in HDL-C levels between FL and DIS are not due to modifications in anthropometric parameters. Prospective studies are needed to better understand the relationship between high-density lipoprotein levels, disability and aging.

Activities of Daily Living↗

Arterial disease in dipper and nondipper hypertensive patients.

Carotid artery and small vessel structural changes were evaluated in 45 dipper and 45 nondipper hypertensive subjects matched for sex, age, body mass index, smoking habit, and serum lipids. Patients underwent carotid ultrasonography to evaluate lumen diameter, intima-media thickness, cross-sectional area, and atherosclerotic plaques, and plethysmographic examination to record minimum forearm vascular resistance. In the whole study population, carotid cross-sectional area and prevalence of atherosclerotic plaques tended to be higher in nondippers than in dippers (19.9 +/- 6.0 v 17.5 +/- 6.1 mm2, P = .07, and 40% v 26%, P = .18), whereas intima-media thickness and minimum forearm vascular resistance were significantly higher in nondippers than in dippers (0.89 +/- 0.12 v 0.8 +/- 0.15 mm, P < .02, and 2.53 +/- 0.3 v 2.34 +/- 0.3 arbitrary resistance units (RU), P < .02). When gender was taken into account, different results were obtained in men and women. In men, vascular characteristics were not significantly different between dippers and nondippers. In women, carotid cross-sectional area and prevalence of atherosclerotic plaques tended to be higher in nondippers than in dippers (18.3 +/- 4.9 v 15.5 +/- 4.5 mm2, P = .06, and 40% v 15%, P = .15), and intima-media thickness and minimum forearm vascular resistance were significantly higher in nondippers than in dippers both before (0.84 +/- 0.1 v 0.73 +/- 0.1 mm, P < .01, and 2.38 +/- 0.3 v 2.16 +/- 0.2 RU, P < .01) and after adjustment for 24-h blood pressure. In conclusion, our data suggest that the progression of vascular disease may be differently affected in the two sexes by a different circadian blood pressure profile.

Blood Pressure Monitoring, Ambulatory↗

White-coat resistant hypertension.

The aim of this study was to evaluate whether sustained hypertensives with high clinic blood pressure, despite multiple drug treatment, show a true resistant hypertension or a "white-coat effect," and whether the pretreatment white-coat effect is maintained despite pharmacological therapy. The occurrence of resistant hypertension was determined in 250 consecutive essential hypertensives who had had an ambulatory blood pressure monitoring before treatment assignment. Twenty-seven of 250 hypertensives with persistently high clinic blood pressure despite 3 months of adequate pharmacological therapy underwent further ambulatory blood pressure monitoring. Using our internal standards, seven patients had a true resistant hypertension whereas 20 subjects showed a large white-coat effect (white-coat resistant hypertension), ie, high clinic blood pressure (> 140/90) but "normal" ambulatory daytime (< 139/90 mm Hg) and 24 h (135/85 mm Hg) blood pressure. Using other cutoff points for ambulatory blood pressure, 134/90 and 135/85 mm Hg for daytime blood pressure, 10 and 13 patients, respectively, were reclassified as true resistant hypertensives and 17 and 14, respectively, were white-coat resistant hypertensives. Interestingly, in white-coat resistant hypertensives the large differences between clinic and ambulatory daytime blood pressure (white-coat effect), recorded before treatment assignment, were not affected by drugs and remained constant over time. Left ventricular mass index in white-coat resistant hypertensives was significantly lower than in truly resistant hypertensives, suggesting that prognosis could differ between these groups. In this study, using either our internal standards or some other cutoffs reported in the literature, the white-coat phenomenon was an important cause of resistant hypertension. The use of ambulatory blood pressure monitoring in these patients may avoid misdiagnosis of resistant hypertension, unnecessary overtreatment, and expensive procedures to look for possible secondary hypertension.

Antihypertensive Agents↗

In vivo formation of 8-Epi-prostaglandin F2 alpha is increased in hypercholesterolemia.

F2-isoprostanes are bioactive prostaglandin (PG)-like compounds that are produced from arachidonic acid through a nonenzymatic process of lipid peroxidation catalyzed by oxygen free-radicals. 8-Epi-PGF2 alpha may amplify the platelet response to agonists, circulates in plasma, and is excreted in urine. We examined the hypothesis that the formation of 8-epi-PGF2 alpha is altered in patients with hypercholesterolemia and contributes to platelet activation in this setting. Urine samples were obtained from 40 hypercholesterolemic patients and 40 age- and sex-matched control subjects for measurement of immunoreactive 8-epi-PGF2 alpha. Urinary excretion of 11-dehydro-thromboxane (TX) B2, a major metabolite of TXA2, was measured as an in vivo index of platelet activation. Low-dose aspirin, indobufen, and vitamin E were used to investigate the mechanism of formation and effects of 8-epi-PGF2 alpha on platelet activation. Urinary 8-epi-PGF2 alpha was significantly (P = .0001) higher in hypercholesterolemic patients than in control subjects: 473 +/- 305 versus 205 +/- 95 pg/mg creatinine. Its rate of excretion was inversely related to the vitamin E content of LDL and showed a positive correlation with urinary 11-dehydro-TXB2. Urinary 8-epi-PGF2 alpha was unchanged after 2-week dosing with aspirin and indobufen despite complete suppression of TX metabolite excretion. Vitamin E supplementation was associated with dose-dependent reductions in both urinary 8-epi-PGF2 alpha and 11-dehydro-TXB2 by 34% to 36% and 47% to 58% at 100 and 600 mg daily, respectively. We conclude that the in vivo formation of the F2-isoprostane 8-epi-PGF2 alpha is enhanced in the vast majority of patients with hypercholesterolemia. This provides an aspirin-insensitive mechanism possibly linking lipid peroxidation to amplification of platelet activation in the setting of hypercholesterolemia. Dose-dependent suppression of enhanced 8-epi-PGF2 alpha formation by vitamin E supplementation may contribute to the beneficial effects of antioxidant treatment.

Antioxidants↗

Impaired glutathione biosynthesis in the ischemic-reperfused rabbit myocardium.

Non-protein thiols (NP-SH) and the activities of the glutathione status-regulating enzymes gamma-glutamylcysteine synthetase (G-GCS), gamma-glutamyl transpeptidase (G-GT) and glutathione reductase (GR) were assessed in perfused rabbit hearts subjected to severe (60 min) or mild (7 min) total ischemia and 30 min reperfusion. Severe ischemia significantly decreased NP-SH, which were further depressed on reperfusion together with a significant decline in G-GCS activity; G-GT and GR activities were unchanged. Specific analytes were unaffected by mild ischemia-reperfusion. Thus, impaired enzymatic biosynthesis of GSH is operative in the reperfused rabbit myocardium after 60 min ischemia. This phenomenon may favour myocardial GSH depression and oxidative reperfusion injury after severe ischemia.

Animals↗

Systemic oxidative stress and its relationship with age and illness. Associazione Medica "Sabin".

OBJECTIVE: It has recently been proposed that increased oxidative stress may play a role in the aging process and age-associated degenerative diseases. DESIGN AND MEASUREMENTS: A cross-sectional study was carried out to assess the relationship of circulating antioxidants, namely vitamins E and C, beta-carotene, proteic thiols (P-SH) and ceruloplasmin, and of lipid peroxides, with both aging and aging with disability, i.e., unsuccessful aging. PARTICIPANTS: One hundred healthy free living and 62 disabled octo-nonagenarians and 91 healthy adults were enrolled in the study. RESULTS: Free living and disabled older adults had lower antioxidant and higher lipid peroxide levels than healthy adults, as well as the disabled older adults compared with free living older persons. Using logistic regression, we observed that plasma concentrations of vitamins E and C, P-SH, and lipid peroxides were independently associated with either aging or aging with disability, apparently representing biochemical indicators of patient status. In particular, aging and unsuccessful aging were associated with higher levels of lipid peroxides independently of circulating levels of vitamins C and E, suggesting that the increased oxidative stress was not merely an effect of a lower dietary intake of antioxidants. Serum ceruloplasmin was significantly higher in free living older adults than in healthy adults, and in the disabled compared with free living octo-nonagenarians. CONCLUSIONS: Our findings are consistent with the presence of systemic oxidant load in older adults, and this phenomenon is far more evident in unsuccessful aging.

Aged↗

Influence of metabolic control on thromboxane biosynthesis and plasma plasminogen activator inhibitor type-1 in non-insulin-dependent diabetes mellitus.

We have previously shown that tight metabolic control by insulin therapy reduced thromboxane-dependent platelet activation in non-insulin-dependent diabetes mellitus (NIDDM) patients. The present study was undertaken to determine whether a similar effect could be obtained without switching diabetics in secondary failure to insulin treatment. For this purpose, we gave strict diet and exercise advise program and adjusted on a weekly basis the oral antidiabetic therapy (glipizide) that 26 patients with NIDDM had been given over the previous months. Basal measurements of urinary 11-dehydro-TXB2 and PAI-1 confirmed previous findings of enhanced levels of these parameters in NIDDM patients with macrovascular disease in comparison to age- and sex-matched controls. After 2-6 weeks, 16 patients achieved tight metabolic control associated with significant reduction of both thromboxane biosynthesis and PAI-1 levels; 10 patients remained in poor control and no significant decrease of both parameters was observed. We conclude that reduction of in-vivo platelet activation and PAI-1 antigen levels after metabolic improvement obtained by frequent reassessment of sulphonylurea therapy together with strict diet and exercise programs may have beneficial effects on the progression of diabetic micro- and macrovascular disease.

Adult↗

The prooxidant properties of captopril.

The thiol drug captopril has been reported to possess reducing and transition metal-binding properties, which could result in specific changes in iron and copper prooxidant capacity. Thus, the effects of captopril on iron- and copper-induced oxidative injury were evaluated using deoxyribose as the oxidizable substrate in the presence of physiological phosphate concentrations but in the absence of the non-physiological chelator EDTA. In an iron(III)/H2O2/ascorbate oxidant system, captopril enhanced deoxyribose oxidation only when it was pre-mixed with iron, whereas it did not influence sugar degradation when not pre-mixed with the metal or when ascorbate was omitted. The physiological thiol GSH acted in a similar manner, whereas the SH-lacking angiotensin-converting enzyme inhibitor ramiprilat did not influence iron-induced deoxyribose oxidation, indicating that the thiol group is crucial in favouring enhanced iron reactivity due to 'malignant' chelation. Further specific experiments designed to evaluate possible thiol-dependent iron(III) reduction failed to demonstrate ferric to ferrous reduction by either captopril or reduced glutathione (GSH). When iron(III) was replaced by copper(II) to induce deoxyribose oxidation, captopril was prooxidant both in the presence and absence of ascorbate, and when pre-mixed or not with copper. On the other hand, GSH was prooxidant up to 2:1 molar ratio with respect to copper but markedly inhibited copper-dependent sugar oxidation beginning at molar ratio of 4:1. Ramiprilat did not significantly influence copper-induced deoxyribose oxidation. Moreover, unlike the experiments performed with iron, captopril, as well as GSH, readily reduced copper(II) to copper(I). Hence, captopril can act as prooxidant in the presence of iron or copper. In the former case, only 'malignant' iron chelation by the drug is involved in oxidant injury, whereas in the latter both copper chelation and reduction are operative, although specific chelating mechanisms are crucial in enhancing copper-induced oxidant injury. Captopril, therefore, cannot be considered simply as an 'antioxidant drug', and its catalytic transition metal-related prooxidant capacity should be taken into account in experimental and clinical investigations.

Captopril↗

Cephalosporins are scavengers of hypochlorous acid.

Potential scavenging properties of cephalosporins (i.e. cefamandole, cefotaxime and ceftriaxone) towards hypochlorous acid (HOCl) as well as the antibacterial activity of control and HOCl-reacted antibiotics were investigated. We found that these drugs, at therapeutically relevant concentrations, are indeed scavengers of HOCl, with ceftriaxone showing the highest anti-HOCl capacity. However, the efficiency of cephalosporins in protecting biological molecules is also related to the chemical identity of such molecules. Indeed, the polyenoic compound beta-carotene is much better protected that the thiol compound GSH against HOCl attack. Moreover, the drugs do not appear to form chloramine derivatives as a result of their reaction with HOCl, and they inhibit taurine-chloramine formation. After HOCl challenge, the antibacterial activity of cefamandole, cefotaxime and ceftriaxone (tested against the standard strain Escherichia coli ATCC 25922) is approx. 8-, 5- and 4-fold lower, respectively, than that of the HOCl-unreacted antibiotics. The depression of the antibacterial activity of cephalosporins appears inversely related to their HOCl scavenging capacity, suggesting that the drug antioxidant groups may protect the beta-lactam ring against HOCl attack. In conclusion, physiological biomolecules are protected by cephalosporins against HOCl-driven oxidative injury with varying efficiency, this antioxidant defence being a consequence of a direct drug scavenging capacity towards HOCl. The interaction of cephalosporins with HOCl, however, results in a depression of their antibacterial activity.

Antioxidants↗

Vitamins E, C and lipid peroxidation in plasma and arterial tissue of smokers and non-smokers.

An imbalance between pro-oxidants and antioxidants is operative in atherosclerosis. Cigarette smoke is a major risk factor of atherosclerosis and has been reported to contain large amounts of oxidants. We assessed arterial (internal mammary artery) and plasma levels of vitamins E and C and lipid peroxides in 48 male patients, 24 smokers and 24 non-smokers, undergoing coronary bypass surgery. Lipid peroxidation was studied using fluorescent products of lipid peroxidation (FPLs). Tissue vitamins E and C levels were significantly lower and FPLs significantly higher in smokers than in non-smokers (P < 0.0006, 0.0005 and 0.0005, respectively). This pattern was associated with lower vitamin C and higher lipid peroxide plasma levels in smokers than in non-smokers (P < 0.0002 and 0.0005, respectively). Vitamins E and C plasma levels were strongly related to their tissue content both in smokers (r = 0.60, P < 0.005 and r = 0.57, P < 0.01) and in non-smokers (r = 0.42, P < 0.05 and r = 0.46, P < 0.05). Moreover, vitamin E content was significantly related to that of vitamin C only in the arterial tissue of both groups, pointing to the existence of a functional interaction between these antioxidants. In both groups, FPLs were significantly and inversely related to vitamin C in plasma and to vitamin E in tissue, suggesting the antioxidant primary of vitamin C and vitamin E in the plasma and arterial tissue compartments, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteries↗

Lipoprotein(a) plasma levels and apo(a) isoforms are not associated with longevity or disability in a sample of Italian octo-nonagenarians. Associazione Medica Sabin.

Cardiovascular diseases are the leading cause of disability and mortality in western countries. Lipoprotein(a) [Lp(a)] is now considered an independent risk factor for atherosclerosis, and might consequently be related to longevity and/or disability. In the context of a study on metabolic and anthropometric parameters in a sample of Italian octo-nonagenarians, Lp(a) and apo(a) isoforms were evaluated. One-hundred and fifty Italian octo-nonagenarians were classified as free-living or disabled, according to Katz's index, and compared to 91 healthy control adults. All the study subjects were recruited from a valley (Val Vibrata valley) near Teramo, in the central part of Italy. The median Lp(a) concentration of the whole group was 17 mg/dL (range 1-161 mg/dL), which is much higher than the values observed in Caucasian populations. No differences were detected between the octo-nonagenarian group (median 16 mg/dL, range 1-126 mg/dL) and the control group (median 19.5 mg/dL, range 1-161 mg/dL), nor between the free-living and the disabled groups. Apo(a) isoforms were similarly distributed among free-living, disabled and control subjects. While our findings suggest that Lp(a) plasma levels and apo(a) isoforms are not factors associated with longevity or disability, we cannot exclude that the low incidence of other major risk factors for atherosclerosis in our free-living octo-nonagenarians hampered the full expression of the lipoprotein(a) atherogenic potential, and thus allowed the achievement of a very old age in a good healthy status, even in carriers of high Lp(a) levels or small apo(a) isoforms.

Adult↗

Intermittent antegrade warm blood cardioplegia.

Intermittent antegrade warm blood cardioplegia has been used routinely at our institution over the last 3 years. We report here a comparison between the first 250 consecutive patients undergoing elective coronary artery bypass grafting in which intermittent antegrade warm blood cardioplegia was used (group A) and the last 250 consecutive patients who received intermittent antegrade cold blood cardioplegia, during bypass grafting (group B). There were no differences in sex, age, number of grafts, and functional status between the two groups; left ventricular ejection fraction was lower in group A. The overall mortality rate in group A was 0.8% versus 3.6% in group B (p < 0.05). There was no in-hospital mortality among high-risk patients (ejection fraction < or = 0.35) in group A (0/53) versus two deaths in group B (2/28) (p < 0.05). No patient in group A needed circulatory assistance; 4 patients in group B received intraaortic balloon pumping. Only 1 patient in group A required inotropic support versus 20 patients in group B (p < 0.0005), and 5 patients in group A received lidocaine hydrochloride for ventricular arrhythmias versus 18 in group B (p < 0.01). The rates of myocardial infarction and stroke were not different between the two groups. The peak concentration of the myocardial-specific isoenzyme of creatine kinase were higher in group B in absolute value (51 +/- 30 IU/L) than in Group A (38 +/- 38 IU/L) (p < 0.0005) and in percent of total creatine kinase (8.2% +/- 4.1% versus 6.2% +/- 2.9%, respectively).

Blood↗

Modulation of rat vascular smooth muscle cell (VSMC) proliferation by cysteinyl leukotriene D4: a role for mediation of interleukin 1.

Recent studies suggest the involvement of inflammatory mechanisms in the progression of atherosclerosis. Cysteinyl leukotrienes and cytokines could orchestrate this progression by acting on the proliferation of vascular smooth muscle cells (VSMC). In cultures of rat VSMC, proliferation was modulated by cysteinyl leukotriene C4 (LTC4) and LTD4, but not LTE4. Co-culturing LTD4 with VSMC produced an increased cell proliferation as assessed by [3H]thymidine incorporation studies (200%) as well as cell counts (70%), using LTD4 at 10(-6)M compared to controls. LTD4 exerted its effect through an interleukin 1 (IL-1)-dependent autocrine regulatory mechanism. When IL-1 was inhibited by using a receptor antagonist (IL-1ra) and a polyclonal antibody to IL-1, we found an inhibition of VSMC proliferation. The increase of VSMC proliferation was associated with the autocrine production of interleukin-1 (IL-1) concomitant to LTD4 stimulation (55.5 +/- 2.5 pg/ml in controls and 177 +/- 0.5 pg/ml in 10(-6)M LTD4). These results may shed new light on the mechanism of inflammatory involvement during atherogenesis, suggesting that the control of cysteinyl leukotrienes may be important in inflammatory processes involving IL-1.

Animals↗

Plasma copper and lipid peroxidation in cigarette smokers.

Plasma levels of copper and lipid peroxidation were evaluated in 14 smokers as compared to 14 nonsmokers. Plasma copper concentrations were higher in smokers than in nonsmokers (122.5 +/- 19.15 vs. 101.5 +/- 16.2 micrograms/dl, P < .01). Plasma lipoperoxidation, evaluated as fluorescent damage products of lipid peroxidation (FDPL), also was higher in smokers than in nonsmokers (20.35 +/- 2.6 vs. 17.1 +/- 2.95 units of relative fluorescence/ml, P < .01). A significant and positive correlation between the number of cigarettes smoked, expressed as pack years, and the levels of either FDPL (r = .61, P < .025) or copper (r = .55, P < .05) was found. Moreover, a significant and positive relationship between copper and FDPL values was observed in smokers (r = .64; P < .025), but not in nonsmokers. These data indicate that cigarette smoke-related plasma oxidant load may be partly due to enhanced levels of the prooxidant metal cooper, potentially suggesting the supplementation of specific antioxidants (e.g., zinc) to counteract cigarette smoke-induced oxidative stress in smokers.

Adult↗