Vitamin K2 is a mitochondrial electron carrier that rescues pink1 deficiency.
Summary of "Vitamin K2 is a mitochondrial electron carrier that rescues pink1 deficiency."
Human UBIAD1 localizes to mitochondria and converts vitamin K(1) to vitamin K(2). Vitamin K(2) is best known as a cofactor in blood coagulation, but in bacteria it is a membrane-bound electron carrier. Whether vitamin K(2) exerts a similar carrier function in eukaryotic cells is unknown. We identified Drosophila UBIAD1/Heix as a modifier of pink1, a gene mutated in Parkinson's disease that affects mitochondrial function. We found that vitamin K(2) was necessary and sufficient to transfer electrons in Drosophila mitochondria. Heix mutants showed severe mitochondrial defects that were rescued by vitamin K(2), and, similar to ubiquinone, vitamin K(2) transferred electrons in Drosophila mitochondria, resulting in more efficient adenosine triphosphate (ATP) production. Thus, mitochondrial dysfunction was rescued by vitamin K(2) that serves as a mitochondrial electron carrier, helping to maintain normal ATP production.
VIB Center for the Biology of Disease, Leuven, Belgium.
This article was published in the following journal.
Name: Science (New York, N.Y.)
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/22582012
- DOI: http://dx.doi.org/10.1126/science.1218632
Medical and Biotech [MESH] Definitions
Vitamin E Deficiency
A nutritional condition produced by a deficiency of VITAMIN E in the diet, characterized by posterior column and spinocerebellar tract abnormalities, areflexia, ophthalmoplegia, and disturbances of gait, proprioception, and vibration. In premature infants vitamin E deficiency is associated with hemolytic anemia, thrombocytosis, edema, intraventricular hemorrhage, and increasing risk of retrolental fibroplasia and bronchopulmonary dysplasia. An apparent inborn error of vitamin E metabolism, named familial isolated vitamin E deficiency, has recently been identified. (Cecil Textbook of Medicine, 19th ed, p1181)
Vitamin D Deficiency
A nutritional condition produced by a deficiency of VITAMIN D in the diet, insufficient production of vitamin D in the skin, inadequate absorption of vitamin D from the diet, or abnormal conversion of vitamin D to its bioactive metabolites. It is manifested clinically as RICKETS in children and OSTEOMALACIA in adults. (From Cecil Textbook of Medicine, 19th ed, p1406)
Vitamin A Deficiency
A nutritional condition produced by a deficiency of VITAMIN A in the diet, characterized by NIGHT BLINDNESS and other ocular manifestations such as dryness of the conjunctiva and later of the cornea (XEROPHTHALMIA). Vitamin A deficiency is a very common problem worldwide, particularly in developing countries as a consequence of famine or shortages of vitamin A-rich foods. In the United States it is found among the urban poor, the elderly, alcoholics, and patients with malabsorption. (From Cecil Textbook of Medicine, 19th ed, p1179)
Vitamin B 12 Deficiency
A nutritional condition produced by a deficiency of VITAMIN B 12 in the diet, characterized by megaloblastic anemia. Since vitamin B 12 is not present in plants, humans have obtained their supply from animal products, from multivitamin supplements in the form of pills, and as additives to food preparations. A wide variety of neuropsychiatric abnormalities is also seen in vitamin B 12 deficiency and appears to be due to an undefined defect involving myelin synthesis. (From Cecil Textbook of Medicine, 19th ed, p848)
Vitamin B 6 Deficiency
A nutritional condition produced by a deficiency of VITAMIN B 6 in the diet, characterized by dermatitis, glossitis, cheilosis, and stomatitis. Marked deficiency causes irritability, weakness, depression, dizziness, peripheral neuropathy, and seizures. In infants and children typical manifestations are diarrhea, anemia, and seizures. Deficiency can be caused by certain medications, such as isoniazid.
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