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Zebrafish may Be Helpful in Studying Mitochondrial Impairments in Humans
Researchers at the University of Oregon claim that their finding has opened an unparalleled pathway to examine the earliest stages of mitochondrial impairments that lead to potentially fatal metabolic disorders.
COX deficiencies refer to a breakdown of cytochrome coxidase, an enzyme located in the mitochondrion of every cell. Mitochondria are crucial cellular workhorses that provide chemical energy. Research of the deficiency has been foiled by a lack of model organisms, with mice being introduced as the first model by Japanese researchers just seven years ago.
COX involves multiple proteins and assembly factors, and deficiencies of any one of them can negatively affect metabolic tissues, including the brain, muscle and eyes. Deficiencies during the prenatal period are considered to be a potential cause of miscarriages and have been led to prenatal screenings.
The comprehensive study, led by doctoral student Katrina N. Baden, could speed research and point to specific targets to test potential drug therapies, said co-author Karen Guillemin, a professor of molecular biology and member of the UO Institute of Molecular Biology.
"Mitochondrial impairments are emerging as important in many human diseases, but there have been few models for understanding exactly what is happening during the early development of the diseases. The use of mice is limited, because knocking out protein expression in mice mitochondria to mimic human-disease states results in large numbers of deaths in utero. Therefore, the symptoms that researchers have wanted to study have not been assessable in mice," Guillemin said.
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