Reduced coenzyme Q(10) in female smokers and its association with lipid profile in a young healthy adult population.

INTRODUCTION: Cigarette smoking has a negative effect on body reserve of antioxidants and cholesterol metabolism. Coenzyme Q(10) (CoQ(10)), a potent antioxidant synthesized as part of the cholesterol pathway, is a potential biomarker for systemic oxidative stress. We aimed to investigate gender variation in plasma lipid profile and CoQ(10) concentrations in healthy non-smokers and in smokers. MATERIAL AND METHODS: The study included 55 cigarette smokers (25 females and 30 males) and 51 non-smokers (25 females and 26 males) with the age range from 21 to 45 years, and who had no history of alcohol abuse or chronic diseases such as diabetes mellitus or obesity. Coenzyme Q(10) plasma concentrations were measured by reverse-phase high performance liquid chromatography (HPLC) with ultraviolet detection. Fasting plasma glucose and lipid levels were determined by standard colorimetric methods. RESULTS: Our results showed that CoQ(10) concentrations were significantly decreased in smokers, especially in females, than their non-smoker counterparts. Female smokers also exhibited a significant decrease in plasma concentrations of total cholesterol (TC), HDL-C, LDL-C, and atherogenic ratios HDL-C/TC and CoQ(10)/LDL-C than male counterparts. Plasma triglyceride concentrations were increased in smokers irrespective of gender. Plasma CoQ(10) was relatively more associated with TC and LDL-C in female smokers than male smokers. CONCLUSIONS: The adverse effects of smoking on body reserve of antioxidants and cholesterol metabolism are greater in females than in males, partially as a result of decreased CoQ(10) plasma concentrations, HDL-C and total-cholesterol and abnormal atherogenicity indices.

Alterations of erythrocyte free radical defense system, heart tissue lipid peroxidation, and lipid concentration in streptozotocin-induced diabetic rats under coenzyme Q10 supplementation.

OBJECTIVE: Free radicals play an important role in genesis and development of various chronic diseases and aging. Our objective is to study the effects of coenzyme Q10 (CoQ10) supplementation on erythrocyte antioxidants, heart tissue lipid peroxidation end products and lipid concentration in different age of diabetic rats. METHODS: In this study, the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and the content of reduced glutathione (GSH) were determined in erythrocytes. The products of lipid peroxidation were determined in the heart tissues of streptozotocin-induced diabetic rats and in healthy rats at 4, 8, and 13-months of age. The above mentioned antioxidant systems of erythrocytes were also determined after supplementation of diabetic and healthy rats with CoQ10. This study was carried out in King Fahad Medical Research Center, Jeddah, Kingdom of Saudi Arabia between 2000 and 2001. RESULTS: In erythrocytes of diabetic rats the activity of GSH-Px was significantly decreased (p<0.001) in all different age groups, whereas the activity of SOD was significantly increased (p<0.001). However, in erythrocyte of streptozotocin-induced diabetic rats, the concentration of GSH and high-density lipoprotein (HDL)-cholesterol were significantly lower than non-diabetic rats. Moreover, the concentration of heart tissue lipid peroxidation end products, and plasma glucose, cholesterol and triacylglycerol were significantly increased (p<0.001) in all age groups of diabetic rats. Daily supplementation with CoQ10 (10 mg/kg body weight, one month) after induction of diabetes to the rats resulted in the following changes: an increase in both erythrocyte GSH concentration and GSH-Px activity, and slightly increases in plasma HDL-cholesterol. However, SOD activity was significantly decreased (p<0.05). In addition, the levels of lipid peroxidation end products, and triacylglycerol were significantly decreased (p<0.05) in diabetic rats supplemented with CoQ10. CONCLUSION: The results of the present study indicated that CoQ10 supplementation helps to prevent clinical complications during the course of the disease in diabetic rats.

Plasma and red blood cells membrane lipid concentration of sickle cell disease patients.

OBJECTIVE: The present study aimed to determine the concentration of plasma and red blood cells (RBCs) membrane lipids in Saudi sickle cell disease (SCD) patients. METHODS: This study was carried out at the Hematology Clinic, King Abdul-Aziz University Hospital, Jeddah, Kingdom of Saudi Arabia from October 1998 to October 1999. Lipid concentrations were determined in plasma and RBC membrane of 81 SCD patients and 66 normal healthy matched individuals (control). Different lipid parameters were measured according to standardized enzymatic assay methods. RESULTS: The plasma concentrations of total cholesterol and low density lipoprotein cholesterol of SCD patients were significantly decreased (p<0.001), whereas the plasma concentrations of high density lipoprotein phospholipids were significantly increased (p<0.001). The plasma concentrations of apo A and apo B were significantly decreased (p<0.001) in SCD patients. However, the concentration of total cholesterol of RBC membrane was significantly increased (p<0.001) in SCD patients, while the phospholipid content was significantly decreased (p<0.001). CONCLUSION: The significant increase of RBC membrane cholesterol concentration in SCD patients possibly is responsible to the change in RBC membrane fluidity that may play a direct role in the sickling phenomenon of RBCs in SCD.

Effect of dietary zinc deficiency on rat lipid concentrations.

OBJECTIVE: Evaluation of the lipid profile in serum, liver, and testis of rats fed marginal and severe zinc deficient diets. METHODS: Three groups of rats were treated for 8 weeks with normal diet, marginally zinc deficient diet and severely zinc deficient diet. Lipid concentrations were measured in serum, liver, and testis of these groups. RESULTS: The concentrations of serum lipids were not significantly altered between marginally zinc deficient diet treated and control rats. However, in rats treated with severely zinc deficient diet, the concentrations of serum total cholesterol, high density lipoprotein cholesterol and phospholipids were significantly increased (P < 0.01) and (P < 0.001), whereas the concentration of triacylglycerol was significantly decreased (P < 0.01). However, low-density lipoprotein cholesterol concentration was non-significantly different from controls. The concentrations of liver total cholesterol, triacylglycerol and phospholipids were significantly decreased (P < 0.001) in rats treated with severely zinc deficient diet. The testicular concentration of total cholesterol was increased but this increase was non-significantly different from controls, whereas the testicular concentrations of triacylglycerol and phospholipids were significantly decreased (P < 0.001) in rats treated with severely zinc deficient diet. CONCLUSION: These results suggest that a marginally zinc deficient diet does not play a significant role in altering rat lipid concentrations. However, the changes in serum lipid concentrations could be related to those changes in tissue lipid concentrations.