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PubMed1992

Simultaneous measurement of serum probucol and lipid-soluble antioxidants.

A method is described for the simultaneous measurement of probucol, retinol, tocopherols, lycopene, and carotenes by reverse phase high performance liquid chromatography. A high sensitivity was achieved by use of a microbore column and by monitoring the effluent at the optimum wavelengths of each substance with a diode array detector. The detection limits were lycopene 0.5 ng; alpha-carotene, beta-carotene, and retinol 1 ng; probucol 2 ng; alpha-tocopherol and gamma-tocopherol 15 ng. The eluent was acetonitrile-water-tetrahydrofuran 81.3:5.7:13 (v/v/v) and the flow rate was 0.4 ml/min. Quantitation was performed by use of the four internal standards retinol acetate, 2-pentanone bis(3,5-di-tert)mercaptole, alpha-tocopherol acetate, and retinol palmitate, which resemble the respective analytes in structure and/or polarity. In order to attain a reproducible recovery of particularly the carotenes, the total lipid content of the samples had to be controlled by dilution of the sample before extraction. The coefficients of variation for between-day determinations of a serum pool were 3.8% for retinol, 4.5% for probucol, 11.2% for gamma-tocopherol, 4.5% for alpha-tocopherol, 10.4% for lycopene, 8.0% for alpha-carotene, and 7.0% for beta-carotene.

Antioxidants↗
PubMed1977

Probucol (Lorelco) in treatment of hyperlipemia.

The chemical structure of probucol differs from that of other hypolipemic agents, and its mechanism of action is unknown. This agent lowers elevated serum cholesterol (and low-density lipoprotein) levels and appears to be effective when used as an adjunct to a low-cholesterol, low-saturated-fat diet for treatment of type IIa hyperlipoproteinimia in adults; however, it is less effective than cholestyramine resin in patients with familial type IIa disorder. Although probucol has no consistent effect on elevated triglyceride levels, it may be useful as an adjunct to other drugs that lower these concentrations in patients with types IIb, III, and IV hyperlipoproteinemia when hypercholesterolemia persists. Probucol is generally well tolerated.

Cholesterol↗
PubMed1989

Antioxidant activity of probucol. Short communication.

To evaluate a possible antioxidant activity of probucol on NADPH-dependent microsomal lipid peroxidation and on iron-doxorubicin (adriamycin) complex-induced phospholipid peroxidation, the effects were compared with another powerful antioxidant, 2-OH-estrone. Antioxidant activity of 10 mumol/l probucol in NADPH-dependent microsomal lipid peroxidation corresponded to 4 mumol/l 2-OH-estrone. Together with the results obtained from iron-doxorubicin complex-induced phospholipid peroxidation, it was concluded that probucol is a potent inhibitor of lipid peroxidation and has one-quarter to one-half the antioxidant activity of 2-OH-estrone in vitro.

Animals↗
PubMed1988

Effectiveness of individualized long-term therapy with niacin and probucol in reduction of serum cholesterol.

A retrospective analysis was made of the results of the individualized office management of hypercholesterolemia in 37 patients (25 male, 12 female) with severe atherosclerosis (n = 35) or a predisposition to it (n = 2). The effects of diet instruction, diet and a niacin supplement, and diet plus the niacin supplement and probucol were assessed. Diet alone (n = 37) was prescribed for an average of 4.8 years; diet plus niacin (n = 37) for an average of 2.0 years; and diet plus niacin and probucol (n = 19) for an average of 2.9 years. Each patient served as his or her own control. The maximum serum cholesterol at the beginning of the diet period was 8.69 +/- 2.15 mmol/L (336 +/- 83 mg/dL) (mean plus or minus standard deviation; n = 37). The goal cholesterol was less than 5.20 mmol/L (200 mg/dL). On diet alone the cholesterol level fell to 7.21 +/- 1.27 mmol/L (279 +/- 49 mg/dL) (P less than .001); and goal cholesterol was reached by 12 of 37 patients (32.4 percent), but was maintained in none. On adding niacin, the mean cholesterol fell to 6.21 +/- 1.16 mmol/L (240 +/- 45 mg/dL) (P less than .001). The goal cholesterol was reached in 22 of 37 patients (59.4 percent), but was maintained in only 7 of 37 (18.9 percent). Nineteen of 37 patients on diet plus niacin also received probucol. Goal cholesterol was reached in 14 of 19 patients (73.6 percent), and was maintained in 11 of 19 (57.9 percent).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

[Effect of probucol on lipid metabolism and the clinical course of ischemic heart disease and arteriosclerosis obliterans of the vessels of the lower extremities].

Thirty-eight men with chronic coronary heart disease (CHD) aged 38 to 65 years (ten patients with attendant obliterating atherosclerosis of lower extremity vessels) were treated with the hypolipidemic drug probucol in a dose of 1000 mg/day for three months. Probucol exerted a beneficial effect on the clinical course of CHD and obliterating atherosclerosis of the lower limb vessels. The drug has a marked hypocholesterolemic effect in CHD patients with high cholesterol levels in the blood serum which warrants the advisability of its use in type IIa and IIb hyperlipoproteinemia. The probucol therapy is associated with a decrease in the cholesterol/erythrocyte membrane phospholipids molar ratio which improves the rheological properties of the blood in CHD patients. The drug produces no side effects.

Adult↗
PubMed1982

Effects of probucol on the cholesterol content of skin in type II hyperlipoproteinemias.

500 mg of probucol were given twice a day for 6 months to 20 type II hyperlipoproteinemic patients, 14 men and 6 women, including 10 type IIb and 10 type IIa cases. Tendon xanthomas were present in 11 and xanthelasma in 4. Their mean blood cholesterol level was 435 +/- 100 mg/100 ml and triglycerides 210 +/- 138 mg/100 ml. A normal diet was maintained during the treatment period. Skin biopsies were made on the forearm, before and after the 6 month treatment. After lyophilization of the skin fragments, the free and esterified cholesterol contents were measured by gas chromatography after preparative thin layer chromatography on silica gel. The free and esterified cholesterol contents of the skin both appear to be significantly increased when the values found before treatment in these patients are compared with those of skin analysis in 10 normal controls: 2.25 to 1.58 micrograms/mg freeze-dried skin, p less than 0.001 for the esterified fraction. After 6 month probucol treatment the free cholesterol does not change significantly (2.25 to 2.16) and the esterified cholesterol increases (0.44 to 0.66, p less than 0.01). This effect is suggestive of an interaction of probucol with the synthesis and transport of cholesterol at the tissue level. It may be significant for the understanding of the effects of this drug and others on xanthelasma, tendon xanthomas, and atherosclerosis. In one of the cases studied here, the xanthelasma was greatly reduced during the treatment.

Cholesterol↗
PubMed1982

Effects of probucol on lipoprotein protein kinetics.

The effects of probucol on the metabolism of low density lipoprotein (LDL) and of high density lipoprotein (HDL) were studied in five hyperlipidaemic subjects. Kinetics of LDL-B protein and HDL-AI protein were determined by two-pool analysis after reinjection of 131I labelled LDL and 125I labelled HDL at the end of placebo and treatment periods. Probucol increased the fractional removal rate of LDL in four, though plasma cholesterol levels fell significantly in only three. The synthesis of HDL-AI protein fell in all and was probably responsible for the uniform reduction in plasma apo-AI levels. Thus, probucol enhances LDL-B protein removal and bile acid excretion but inhibits AI protein formation.

Apolipoproteins↗
PubMed1980

[Probucol: mechanism of action (author's transl)].

The mechanism of action of probucol is discussed after human and animal studies. This drug seems to have a poor or no effect on the overall cholesterol synthesis in the body and does not produce any storage of cholesterol or its metabolic intermediates (i.e. desmosterol) in the tissues. The main effect of probucol could be a decreased synthesis and/or an acceleration of plasma lipoprotein turnover; disappearance of xanthomatous lesions under traitement suggest a facilitation of cholesterol transferred from tissues to the excretion or catabolic pathways; its relevance in atheroma lesions is to be proved. Probucol seems to be a non hepatotoxic drug and induces a decrease of lithogenic index of bile.

Animals↗
PubMed1980

[Prolonged probucol treatment in patients with cardiovascular diseases (author's transl)].

Thirty five patients with cardiovascular diseases and hypercholesterolemia were treated with probucol and a low-fat diet for 12 to 50 months. The mean serum cholesterol level decreased from 327,2 to 279,4 mg/dl (- 14,6% p. < 0,001). Probucol lowered the plasma cholesterol level by about the same extent in primary hypercholesterolemia type IIa (10 patients) and in combined hypercholesterolemia type IIb or III (23 patients). No interaction was observed between probucol and other drugs prescribed for cardiovascular diseases particularly antivitamin K and diuretics. No variation in liver and renal function tests, in glucose level, blood count or body weight were noted. The E.C.G. was not modified by treatment. The therapy was withdrawn in one patient because of diarrhea.

Adult↗
PubMed1980

[Comparative effects of probucol and placebo on blood cholesterol in patients on long-term treatment (author's transl)].

Male patients were given long-term treatment with probucol, and the effects of the drug were compared with those of placebo. Probucol lowered plasma cholesterol levels, and this action was sustained with time; it had no significant effect on triglycerides. The only adverse reaction of some clinical import was bouts diarrhea, which did not usually require withdrawal of the drug. In view of these results and of the death figures during the observation period, the authors envisage to undertake a larger scale study of secondary prevention of mortality in patients with coronary disease treated with probucol.

Cholesterol↗
PubMed1980

Usefulness of probucol in treating primary hypercholesterolemia.

Probucol (1 g per day) was administered in a double-blind crossover trial to 16 patients with familial hypercholesterolemia who had previously been tested for their response to clofibrate. Probucol led to a fall in the plasma cholesterol concentration of 15% or more (mean 20.2%) in 5 of the 12 clofibrate-resistant patients and between 8% and 15% in 3 others. The reduction was statistically significant in 7 of these 12 patients as well as in 3 of the 4 patients sensitive to clofibrate. Thus, probucol has a place in the treatment of patients with primary hypercholesterolemia who do not respond to clofibrate.

Adult↗
PubMed1994

Clinical investigation on the hypolipidemic effect of simvastatin versus probucol in hemodialysis patients.

In chronic renal failure hypertriglyceridemia is a well-known complication that persists during hemodialysis treatment: it may be one of the major risk factor for cardiovascular death in these patients. We studied the effects of two lipid lowering drugs; simvastatin (20 mg/day for six months) and probucol (500 mg/day for six months), on lipid profile in 12 hemodialysis patients. Simvastatin therapy reduced plasma total cholesterol by 26% (p > 0.002), LDL-cholesterol by 36% (p > 0.002) and triglycerides by 28% (p > 0.05): plasma HDL-cholesterol and apo-A were raised, but not significantly. Probucol therapy decreased plasma triglycerides by 38% (p > 0.05), total cholesterol by 15% and LDL-cholesterol by 19%: plasma HDL-cholesterol and apo-A were decreased but not significantly. No side effects occurred with either drug. These data suggest that in hemodialysis patients both simvastatin and probucol profoundly affect the lipid profile, as well as the triglyceride levels.

Aged↗
PubMedDate not supplied

Probucol therapy in the prevention of restenosis after successful percutaneous transluminal coronary angioplasty.

The effect of probucol, a drug that inhibits the secretion of smooth muscle cell-derived growth factor, was evaluated in the prevention of restenosis after percutaneous transluminal coronary angioplasty (PTCA). In 67 patients who successfully underwent prospective PTCA for the first time, the effects obtained in 31 patients given 750 mg or 1000 mg of probucol daily (group P) were compared with those in 36 patients given 150 mg of dipyridamole daily (group D). Drug treatment was initiated at least 7 days before PTCA and was continued for 3 to 6 months after PTCA, at which time a follow-up angiography was performed. There were no significant differences in patient characteristics (age, sex, pre-PTCA severity of angina pectoris), the number of affected vessels undergoing dilatation, or the residual degree of stenosis. The restenosis rate was significantly lower in group P (6 cases, 19.4%) than in group D (15 cases, 41.7%). In the nonrestenosis subgroup, the degree of stenosis progressed from 28.0 +/- 13.9% just after PTCA to 32.4 +/- 20.5% at follow-up angiography in group P, while it progressed significantly from 28.6 +/- 15.6% to 40.1 +/- 21.2% in group D (P < 0.05). A significant drop in serum cholesterol was observed in group P. The restenosis rate was lower in patients with high cholesterol levels at PTCA. No adverse reactions were noted in any patient. We conclude that probucol is effective in preventing restenosis after PTCA.

Aged↗
PubMed1997

[The antioxidant probucol as a regulator of the intensity of free-radical lipid peroxidation processes in the blood of patients with coronary atherosclerosis].

Two series of studies were made to assess probucol medicines (lipomal, "Alkaloid"; fenbutol "Akrikhin") effect on clinical symptoms, lipid metabolism, primary and secondary products of lipid peroxidation, activity of antioxidant enzymes (superoxide dismutase, glutathione peroxidase) in atherosclerotic patients with hyperlipidemia type IIA and IIB. In both series probucol reduced frequency of anginal attacks, content of total cholesterol and LDL cholesterol. HDL cholesterol remained unchanged or reduced insignificantly. Lipoperoxides and malonic dialdehyde levels in plasma progressively lowered against activation of antioxidant enzymes. These biochemical parameters returned to initial values within 3 months since the drug discontinuation. It is evident that antiatherogenic effect of probucol is due to indirect activation of natural defense systems responsible for enzymic detoxication of active oxygen forms and lipoperoxides rather than to direct interaction of this synthetic antioxidant with lipid radicals.

Antioxidants↗
PubMed1984

Pharmacokinetics of probucol in male rats.

The bioavailability and pharmacokinetic behavior of 10 mg/kg of [14C]probucol in an oil-water emulsion was determined after oral and intravenous administration to rats. The bioavailability of the oral formulation was approximately 6%. For the first 12-h interval after the intravenous bolus, plasma probucol concentrations increased after an initial decrease. This effect may be attributed to the formulation or precipitation of the drug in the vasculature. The terminal plasma half-life was 6 d. By 7 d, 45 and 4.65% of the labeled intravenous bolus was excreted in the feces and in the urine, respectively. Although most of the labeled dose was excreted in the bile, any enterohepatic recirculation that did occur did not contribute to the atypical plasma concentration versus time profile. The tissue distribution of the label and elimination rates in the bile differed between the two routes of administration. Either the total body burden, precipitation of the drug, or the emulsion vehicle may be responsible for the nonlinear distribution and clearance of the intravenous dose.

Animals↗
PubMed2000

Vitamin E and probucol reduce urinary lipophilic aldehydes and renal enlargement in streptozotocin-induced diabetic rats.

Diabetes mellitus is characterized by complications affecting several organs, including the kidney. Lipid peroxidation increases in diabetes and has been implicated in the pathogenesis of diabetic complications. In this study, we examined the ability of two antioxidants, vitamin E and probucol, to reduce lipid peroxidation in vivo and renal hypertrophy, an early stage of diabetic nephropathy, in rats. Animals were divided into four groups: non-diabetic, diabetic, diabetic treated with vitamin E, and diabetic treated with probucol. Animals were given antioxidants by intraperitoneal injection after induction of diabetes by streptozotocin injection. After 7 wk, lipid peroxidation in vivo was measured by analyzing urinary excretion of lipophilic aldehydes and related carbonyl compounds (LACC) as 2,4-dinitrophenylhydrazones by high-performance liquid chromatography. A number of urinary lipophilic nonpolar and polar aldehydes and related carbonyl compounds were identified, almost all of which increased in diabetes. Antioxidant treatment resulted in significantly decreased excretion of urinary LACC excretion. Antioxidant treatment of diabetic rats reduced renal hypertrophy. There was a high correlation between kidney weight and urinary LACC. Since LACC are accepted markers of lipid peroxidation, these results indicate that antioxidants can reduce the elevated lipid peroxidation of diabetes and may slow the onset of diabetic nephropathy.

Aldehydes↗
PubMed2000

Probucol.

The purpose of this review article is twofold. It seeks to present an overview of research studies conducted on the many effects of probucol, and it demonstrates the interest in pursuing studies on probucol"s multiple specific actions and its future as a therapeutic agent. Within this article, the results of animal studies, experimental human studies, and clinical human studies are detailed, as is information on toxicology studies and on the side effects of the drug.

Animals↗
PubMed1983

Influence of clofibrate, bile-sequestering agents and probucol on high-density lipoprotein levels.

The management of lipid disorders has been greatly improved by advances in our understanding of lipoprotein metabolism. New developments in the isolation and quantitation of the lipoprotein apoproteins have shed light on their essential role in normal and abnormal lipid transport and have helped clarify the mode of action of lipid-lowering drugs. Excess lipid levels can occur because of overproduction, faulty degradation or defective removal of 1 or more lipoproteins. Clofibrate appears to decrease levels of very low density lipoproteins (VLDL) and intermediate-density lipoproteins (IDL) by enhancing their intravascular degradation. Although it often slightly decreases low-density lipoprotein (LDL) levels, it may markedly increase LDL levels in patients with initially high VLDL levels. Its effects on high-density lipoproteins (HDL) are small, often increasing HDL slightly. Bile acid sequestrants act by enhancing the rate of removal of LDL. Their effects on VLDL and IDL are slight. In some subjects there is a moderate increase in both VLDL and IDL levels. HDL concentrations are increased minimally. Probucol's mechanism of action is still unclear, but it appears to enhance LDL removal. Its effects on VLDL and IDL are minimal. Of concern is the repeated observation that probucol reduces HDL concentrations by decreasing HDL synthesis. The resultant reduction in HDL concentrations often rivals its effect in decreasing LDL levels. Knowledge of the selective effect of lipid-lowering drugs on specific lipoprotein fractions is essential for their proper therapeutic selection.

Bile Acids and Salts↗