Lipid metabolism in rats is modified by nitric oxide avilability through a Ca++-dependent mechanism.

MARRA CARLOS A; NELLA, JULIO; MANTI, DAMIÁN; ALANIZ, MARÍA J. TACCONI DE

LIPIDS

American Oil Chem Soc. Press

Año: 2006 vol. 42

0024-4201

We studied lipid metabolism and antioxidant defense system in plasma and liver of rats fed diets supplemented with Lw-nitro-L-arginine methyl ester (L-NAME), isosorbide dinitrate (DIS), L-arginine (Arg), or the associations of these drugs. Liver hydroperoxides and 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 [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 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, DIS. However, predominating phopspholipid synthesis increased the neutral/polar ratio. Decreased levels of NO (low [Ca++]) was directly associated to increased fatty acid synthetase, decreased phospholipase A2, carnitine-palimitoyl transferase, and fatty acid desaturase activities. Raised NO (high [Ca++]) inversely correlated with increased phospholipase-A2 and acyl-CoA-synthetase, and decreased fatty acid synthetase and b-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.