Mrp: 260INR (Syp) 285INR (cap)
L-ornithine-L-aspartate acts on two key ammonia detoxification pathways, urea synthesis and glutamine synthesis, via the amino acids ornithine and aspartate. Urea synthesis takes place in the periportal hepatocytes, in which ornithine serves both as an activator of the two enzymes (ornithine carbamoyl transferase and carbamoyl phosphatase synthetase) and as a substrate for urea synthesis. Glutamine synthesis is localized in the perivenous hepatocytes. Under pathological conditions in particular, aspartate and other dicarboxylates, including metabolic products of ornithine, are taken up into the cells where they are used in the form of glutamine to bind ammonia. Both physiologically and pathophysiologically glutamate serves as an ammonia-binding amino acid. The resulting amino acid glutamine not only provides a nontoxic form for the excretion of ammonia but also activates the important urea cycle (intercellular glutamine exchange).
Silymarin, a flavonolignan from ‘milk thistle’ (Silybum marianum) plant is used from ancient times as a hepatoprotective drug. Along with hepatoprotective action other actions includes antioxidant, anti-lipid peroxidative, antifibrotic, anti-inflammatory, immunomodulatory and liver regenerating.
Silymarin is an antioxidant and free radical scavenger. It can also interact directly with the cell membrane components to prevent any abnormalities in the content of lipid fraction responsible for maintaining normal fluidity. The mechanism of free radical damage includes ROS- induced peroxidation of polyunsaturated fatty acid in the cell membrane bilayer, which causes a chain reaction of lipid peroxidation. Lipid peroxidation is caused by interaction of free radicals with unsaturated fatty acids in lipids resulting in broad spectrum alterations and the consequent degeneration of cell membranes. Silymarin appears to act as an antioxidant not only because it acts as a scavenger of free radicals that induce lipid peroxidation but also it influences enzyme systems associated with glutathione and superoxide dismutase.
Due to the poor solubility of silymarin, it is administered in the form of encapsulation sugar coated tablets. About 20-40% of the administered dose of silymarin is excreted in bile as sulphates and glucuronide conjugates. The peak plasma concentration is achieved in 6 to 8 hrs and its elimination half life is approximately 6hrs. It is mainly excreted as metabolites in the bile and is subject to enterohepatic circulation.
One tablespoonful BD for syrup
One capsule Twice a day
No interaction studies have been performed. Up to now, interactions are not known.