DNP causes mitochondrial malfunction, limits mitochondrial ATP generation, and hinders normal mitochondrial output increases throughout development. The rates of in vivo respiration (oxygen consumption) in intact zebrafish embryos were studied. Oxygen consumption was measured using a Clark-type electrode. Results showed that basal oxygen consumption was not affected by DNP treatment, whereas maximal respiratory capacity was significantly decreased. These findings indicate that DNP inhibits electron transport at the level of complex III and reduces ATP synthesis through the oxidative phosphorylation pathway.
As it is absorbed into mitochondrial membranes, DNP progressively limits electron transport. The effects appear to be dependent on DNP and mitochondrial concentrations, and they differ from one preparation to the next. DNP was marketed as a successful diet medication in the 1930s. It was prescribed by doctors to help weight loss and control blood sugar for patients with diabetes.
Today, the only use of DNP is as an animal feed additive. It is used at levels well below those that cause toxic effects in animals. When administered to pigs, cats, and dogs, for example, it reduces weight gain without affecting food consumption.
DNP inhibits carnitine palmitoyltransferase I (CPT-I), an enzyme responsible for converting fatty acids into energy. CPT-I is found in the mitochondria of body cells; it receives a command from the cell's nucleus to create energy from fat molecules. In humans and other mammals, this process occurs primarily in the liver and muscles. Drugs that inhibit CPT-I force these cells to burn down their own fat stores. Over time, this can lead to weight loss because there are no new fats being synthesized to replace the ones lost.
When used as a growth promoter in livestock, DNP is added to the animals' food or water. This prevents them from losing weight while they build up muscle mass.
Mitochondria play a critical function in cellular respiration by producing ATP from chemical energy present in glucose and other substances. Mitochondria are also responsible for the formation of iron and sulfur clusters, which serve as cofactors for numerous enzymes. Impairment of mitochondrial function has been linked to many diseases.
The mitochondrion is the power plant of cells. It creates energy for our bodies by transforming nutrients into adenosine triphosphate (ATP). This process is called oxidative phosphorylation. The mitochondrion is also involved in other important functions for cells: it produces hormones such as insulin and cortisol, controls cell division, and kills cells if they are no longer needed. Damaged or defective mitochondria may cause inherited disorders known as mitochondrial diseases. Accumulation of these defects over generations leads to widespread damage of tissues that can result in death.
The glycolysis pathway is the biochemical reaction by which carbohydrates are broken down into simple sugars that can be used by cells for growth and maintenance. Glycolysis converts glucose into pyruvate, which can then be converted into acetyl-CoA, which enters the TCA cycle. This pathway requires oxygen, so cannot take place inside cells. Instead, under normal conditions, most cells rely on oxidative phosphorylation for their energy needs.
Cellular respiration is a metabolic mechanism that converts glucose into ATP. Glycolysis, pyruvate oxidation, the citric acid or Krebs cycle, and oxidative phosphorylation are all steps of cellular respiration. In mammals, these processes occur in cells containing mitochondria, resulting in the release of energy in the form of ATP.
ATP is the master molecule that allows cells to function. It provides the potential energy for all biological processes including moving molecules around inside cells, activating enzymes, contracting muscles, etc. When we eat foods that contain carbohydrates, they are broken down into their component parts - sugars - which are used by cells to produce energy. This occurs through two processes: glycolysis and the citric acid cycle. These processes result in the production of high-energy phosphate bonds that can be converted into ADP which can then be used to create more ATP. The overall process is called cellular respiration.
When we look at how we produce ATP from food, there are really three main pathways: the glycolytic pathway, the tricarboxylic acid (TCA) cycle, and electron transport chain (ETC) reactions. Each pathway produces one net atom of oxygen per atom of carbon consumed; therefore, they all result in the removal of oxygen atoms from living systems.
Mitochondria use oxygen from within the cell to transform chemical energy from food into energy used by the host cell. NADH is subsequently converted to adenosine triphosphate by enzymes contained in the mitochondrial inner membrane (ATP). The energy in ATP is stored in the form of chemical bonds. As such, it can be used to do work such as move an object or open a lock.
The process requires several proteins contained in the mitochondrion and some additional proteins located in the cytoplasm. RNA molecules also play a role by coding for certain proteins. Effective treatment of disease caused by defects in mitochondrial function therefore requires not only identification of the molecular defect, but also delivery of appropriate therapy to correct it.
Foods that are good sources of nutrients needed for mitochondrial function include vegetables, fruits, whole grains, and dairy products. Eating enough nutritious food will provide your body with what it needs to keep mitochondria healthy.
Also see: Mitochondrial Disease.