L-arginine supplement, the natural protection from cardiovascular disease: unraveling the biochemical mechanisms

To evaluate the anti-atherosclerotic effect of 'L-arginine and to unravel the biochemical mechanisms involved in this phenomenon. The effect of L-arginine is compared with nitroglycerin [NO donor] and enalapril [ACE inhibitor]. New Zealand white rabbits were rendered hypercholesterolemic by feeding 2% cholesterol rich diet for 28 days. Treated rabbits were given L-arginine [2.25 gm% in drinking water], nitroglycerin [175 mg orally on every day from day 15 to 27] or enalapril [3mg/kg orally] in conjunction with the 2% cholesterol enriched diet. The parameters measured were serum lipid profile, MDA, NO levels and Dimethylarginine dimethylaminohydrolase and ACE activities. Furthermore, aortic ACE activity and platelet aggregation were estimated. Histopathological examination and measurement of the intimal thickness of aorta were also performed. Although L-arginine, nitroglycerin and enalapril didn't significantly modify the lipid profile altered by hypercholesterolemia, they positively modified the parameters that were involved in atherogenesis. Reduction of serum MDA levels, serum ACE activities, platelet aggregation and aortic intimal thickness were achieved in all treated groups. L-arginine and nitroglycerin treatment were shown to increase serum NO levels. L-arginine and enalapril effectively inhibited aortic ACE activities. L-arginine supplementation exhibits anti-atherosclerotic properties very similar to those shown for the cardiovascular drugs, nitroglycerin and enalapril, thus its intake represents a potentially novel nutritional strategy for preventing cardiovascular diseases and their complications

Effect of melatonin with vitamin E or verapamil on kainate-induced lipid peroxidation in rat brain

This work aimed to study the in vivo protective effect of melatonin [Mel] alone or in combination with either vitamin E [Vit E] or verapamil [Ver] against lipid peroxidation that induced by kainic acid [KA] in rat brain. KA was given in a single dose of either 5 mg/kg [LoKA] or 10 mg/kg [HiKA]. Mel [10 mg/kg] was injected three times every eight hours before KA administration. Vit E [200 mg/kg] or Ver [10 mg/kg] was injected once daily for seven days before KA. The protective effect of their combination with Mel was tested. The whole brain malondialdehyde [MDA] was assessed as an index of lipid peroxidation as well as the antioxidants; namely, glutathione peroxidase activity [GProx] and reduced glutathione [GSH]. It was shown that KA increased brain MDA content and GProx activity, while GSH level was decreased, and these effects were more pronounced with HiKA

Some biochemical screening tests of metabolic disorders in Egyptian children suffering mental retardation

The present study deals with investigation of the biochemical abnormality and the metabolic disorders which may be the cause or contribute significantly to the cause of mental retardation [MR]. The study included 203 mentally retarded children who were subjected to qualitative chemical tests on urine for the detection of certain defects in amino acid and carbohydrate metabolism. Thin layer chromatographic detection of specific amino acids in plasma and urine, and the quantitative determination of urea, creatinine, ammonia and uric acid in plasma, argininosuccinase and argininase enzyme activities in erythrocytes; mucopolysaccharides and creatinine in urine were also investigated. It was found that in 92 patient, mental retardation is accompanied by metabolic disorders. These comprise disorders in amino acid transport [10.6%] urea cycle abnormalities [17.4%], generalized amino acid urea [10.8%], miscellaneous aminoacidopathies [25%] and defects in carbohydrate metabolism [26.1%]. The plasma levels of urea, uric acid and creatinine in patients with disorders in aminoacid transport were unchanged indicating normal kidney function. Patients with urea cycle abnormalities showed deficiency in different enzymes controlling urea formation with elevation in plasma ammonia and decrease in plasma urea. Patient with carbohydrate metabolism disorders showed increased urinary mucopolysaccharides. These metabolic disorders were discussed on the basis of the findings obtained and the genetic defect that led to the respective metabolic disorder. According to results of this work, it is highly recommended to carry out genetic counselling in calculating the possibilities for recurrence risk of hereditary disorders and in detecting any metabolic abnormality to prevent the onset of mental retardation. Early detection of these cases and evaluation of specific treatment will be valuable for the management of these cases