• Anti bacterial

• Metabolism: Capric acid (decanoic acid) is rapidly metabolized by the β-oxidative pathway, giving rise to C8- and C6-dicarboxylic acids (T29). The enzyme MCAD (medium-chain acyl-CoA dehydrogenase) is responsible for the dehydrogenation step of fatty acids with chain lengths between 6 and 12 carbons as they undergo beta-oxidation in the mitochondria. Fatty acid beta-oxidation provides energy after the body has used up its stores of glucose and glycogen. This typically occurs during periods of extended fasting or illness when caloric intake is reduced, and energy needs are increased. Beta-oxidation of long chain fatty acids produces two carbon units, acetyl-CoA and the reducing equivalents NADH and FADH2. NADH and FADH2 enter the electron transport chain and are used to make ATP. Acetyl-CoA enters the Krebs Cycle and is also used to make ATP via the electron transport chain and substrate level phosphorylation. When the supply of acetyl-CoA (coming from the beta-oxidation of fatty acids) exceeds the capacity of the Krebs Cycle to metabolize acetyl-CoA, the excess acetyl-CoA molecules are converted to ketone bodies (acetoacetate and beta-hydroxybutyrate) by HMG-CoA synthase in the liver. Ketone bodies can also be used for energy especially by the brain and heart; in fact they become the main sources of energy for those two organs after day three of starvation. (Wikipedia)
• Uses/Sources: Capric acid occurs naturally in coconut oil (about 10%) and palm kernel oil (about 4%), otherwise it is uncommon in typical seed oils. It is found in the milk of various mammals and to a lesser extent in other animal fats. Capric acid is used in the manufacturing of esters for artificial fruit flavors and perfumes. It is also use as an intermediate in chemical syntheses. It is used in organic synthesis and industrially in the manufacture of perfumes, lubricants, greases, rubber, dyes, plastics, food additives and pharmaceuticals. (Wikipedia)
• Health Effects: Octanoic (OA) and decanoic (DA) acids are the predominant metabolites accumulating in medium-chain acyl-CoA dehydrogenase (MCAD; E.C. 1.3.99.3) deficiency (MCADD), the most common inherited defect of fatty acid oxidation. Glycine and l-carnitine bind to these fatty acids giving rise to derivatives that also accumulate in this disorder. The clinical presentation typically occurs in early childhood but can occasionally be delayed until adulthood. The major features of the disease include hypoglycemia, vomiting, lethargy and encephalopathy after fasting, infection or other metabolic stressors. (A15457)
• Symptoms: MCADD presents in early childhood with hypoketotic hypoglycemia and liver dysfunction, often preceded by extended periods of fasting or an infection with vomiting. Infants who are exclusively breast-fed may present in this manner shortly after birth, due to poor feeding. In some individuals the first manifestation of MCADD may be sudden death following a minor illness. A number of individuals with MCADD may remain completely asymptomatic, provided they never encounter a situation that sufficiently stresses their metabolism. (Wikipedia) Irritating to the skin, lung, or gastrointestinal tract, depending on the route of exposure (MSDS).
• Treatment: Management of acute MCADD includes rapid correction of hypoglycemia, rehydration and treatment of the underlying infection or other stress factor. Current long-term therapy includes avoidance of fasting and a high carbohydrate low-fat diet, but it does not fully prevent the crises and the neurological alterations. (A15457)
• Route of Exposure: Dermal (MSDS) ; eye contact (MSDS) ; inhalation (MSDS); oral (MSDS)

• Carcinogenicity: No indication of carcinogenicity (not listed by IARC). (L135)
• Toxicity: LD50: 3730 mg/kg (Oral, Rat) (MSDS) LD50: 1770 mg/kg (Dermal, Rabbit) (MSDS)

It has been demonstrated that octanoic (OA) and decanoic (DA) acids compromise the glycolytic pathway and citric acid cycle functioning, increase oxygen consumption in the liver and inhibit some activities of the respiratory chain complexes and creatine kinase in rat brain (A15454, A15455). These fatty acids were also shown to induce oxidative stress in the brain (A15456). Experiments suggest that OA and DA impair brain mitochondrial energy homeostasis that could underlie at least in part the neuropathology of MCADD. (A15457)