词条 | mitochondrion |
释义 | mitochondrion biology ![]() ![]() Most of the proteins and other molecules that make up mitochondria originate in the cell nucleus. However, 37 genes (gene) are contained in the human mitochondrial genome, 13 of which produce various components of the ETC. Mitochondrial DNA (mtDNA) is highly susceptible to mutations (mutation), largely because it does not possess the robust DNA repair mechanisms common to nuclear DNA. In addition, the mitochondrion is a major site for the production of reactive oxygen species (ROS; or free radicals (radical)) due to the high propensity for aberrant release of free electrons. While several different antioxidant proteins within the mitochondria scavenge and neutralize these molecules, some ROS may inflict damage to mtDNA. In addition, certain chemicals and infectious agents, as well as alcohol (alcoholic beverage) abuse, can damage mtDNA. In the latter instance, excessive ethanol (alcohol) intake saturates detoxification enzymes, causing highly reactive electrons to leak from the inner membrane into the cytoplasm or into the mitochondrial matrix, where they combine with other molecules to form numerous radicals. In many organisms, the mitochondrial genome is inherited maternally. This is because the mother's egg cell donates the majority of cytoplasm to the embryo, and mitochondria inherited from the father's sperm are usually destroyed. There are numerous inherited and acquired mitochondrial diseases. Inherited diseases may arise from mutations transmitted in maternal or paternal nuclear DNA or in maternal mtDNA. Both inherited and acquired mitochondrial dysfunction is implicated in several diseases, including Alzheimer disease and Parkinson disease (parkinsonism). The accumulation of mtDNA mutations throughout an organism's life span are suspected to play an important role in aging, as well as in the development of certain cancers (cancer) and other diseases. Because mitochondria also are a central component of apoptosis (programmed cell death), which is routinely used to rid the body of cells that are no longer useful or functioning properly, mitochondrial dysfunction that inhibits cell death can contribute to the development of cancer. The maternal inheritance of mtDNA has proved vital to research on human evolution and migration (human migration). Maternal transmission allows similarities inherited in generations of offspring to be traced down a single line of ancestors for many generations. Research has shown that fragments of the mitochondrial genome carried by all humans alive today can be traced to a single woman ancestor living an estimated 150,000 to 200,000 years ago. Scientists suspect that this woman lived among other women but that the process of genetic drift (chance fluctuations in gene frequency that affect the genetic constitution of small populations) caused her mtDNA to randomly supersede that of other women as the population evolved. Variations in mtDNA inherited by subsequent generations of humans have helped researchers decipher the geographical origins, as well as the chronological migrations of different human populations. For example, studies of the mitochondrial genome indicate that humans migrating from Asia to the Americas 30,000 years ago may have been stranded on Beringia, a vast area that included a land bridge in the present-day Bering Strait, for as long as 15,000 years before arriving in the Americas. |
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