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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Lipid Metabolism in Rats is Modified by Nitric Oxide Availability Through a Ca(++)-Dependent Mechanism.

We studied lipid metabolism and the antioxidant defense system in plasma and liver of rats fed diets supplemented with L: (omega)-nitro-L: -arginine methyl ester (L: -NAME), isosorbide dinitrate (DIS), L: -arginine (Arg), or the associations of these drugs. Liver hydroperoxide and thiobarbituric-acid-reactive substance (TBARS) levels were decreased by Arg and increased by L: -NAME or DIS treatments. Oxidized glutathione and conjugated dienes were increased by DIS. Nitrate + nitrite levels and serum calcium ([Ca(++)]) were incremented by Arg or DIS and reduced by L: -NAME. Superoxide dismutase and catalase activities decreased under Arg treatment, while L: -NAME or DIS caused stimulation. Liver high-density lipoprotein (HDL) cholesterol was increased by DIS or NAME (alone or associated with Arg). Free fatty acids and neutral and polar lipids were increased by Arg, L: -NAME, and DIS. However, predominating phospholipid synthesis increased the neutral/polar ratio. Decreased levels of nitric oxide (NO) (low [Ca(++)]) was directly associated with increased fatty acid synthetase, decreased phospholipase A(2), carnitine-palmitoyl transferase, and fatty acid desaturase activities. Raised NO (high [Ca(++)]) inversely correlated with increased phospholipase-A(2) and acyl-coenzyme A (CoA) synthetase and decreased fatty acid synthetase and beta-oxidation rate. Arg or DIS produced changes that were partially reverted by association with L: -NAME. Based on these observations, prolonged therapeutical approaches using drugs that modify NO availability should be carefully considered.[1]

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