For the long story on mitochondria see: http://en.wikipedia.org/wiki/Mitochondria In the short term we are concerned with our energy factories numbering anywhere from 200 to 2,000 per everyone of your approximately one hundred trillion cells, you didn’t know?
Even as a scientist one finds it somewhat difficult to even imagine a production unit so infinitely small. But they are there, and take up about 80% of the oxygen we breath and importantly rely on up to 90 nutrients to produce our energy .
And how is that achieved? The food we eat is oxidized to produce high-energy electrons that are converted to stored energy. This energy is stored in high energy phosphate bonds in a molecule called adenosine triphosphate, or ATP. ATP is converted from adenosine diphosphate by adding the phosphate group with the high-energy bond. Various reactions in the cell can either use energy (whereby the ATP is converted back to ADP, releasing the high energy bond) or produce it (whereby the ATP is produced from ADP). So there you have it but apologies for the gobbledygook, there is no easier way and in our case does not matter. What matters is: ATP production in the mitochondria generates free radicals which can cause localised oxidative stress and damage the mitochondria. By the way your mitochondrion have their very own DNA.
But first, one-up for the femmes: In mammals, 99.99% of mitochondrial DNA (mtDNA) is inherited from the mother. This is because the sperm carries its mitochondria around a portion of its tail and has only about 100 mitochondria compared to 100,000 in the oocyte. As the cells develop, more and more of the mtDNA from males is diluted out. Hence less than one part in 104 or 0.01% of the mtDNA is paternal. This means that mutations of mtDNA can be passed from mother to child. Congratulations ladies! But then you always knew your superiority ladies didnya?
The mitochondria are the only place in the cell where oxygen can be combined with the food molecules. After the oxygen is added, the material can be digested. They are working organelles that keep the cell full of energy. A mitochondrion may also be involved in controlling the concentration of calcium (Ca) within the cell.
Antioxidants protect the mitochondria against oxidative stress by acting as free radical scavengers and are therefore vital for all energy-dependant processes, including heart muscle contraction. Supplementing with specific nutrients may help build up the body’s energy reserves and may improve stamina and endurance.
The heart is the most susceptible of all the organs to premature ageing and oxidative stress; free radical induced damage is believed to contribute to cardiovascular disease through a number of pathways.
Damage - and subsequent dysfunction – through a wide variety of determinants in mitochondria is an important factor in a wide range of human diseases. Mitochondrial disorders often present as neurological disorders, but can manifest as myopathy, (muscle disorders) diabetes, multiple endocrinopathy, (all or any of your glands) or a variety of other systemic manifestations, and very importantly all autoimmune diseases.
Environmental influences may also interact with hereditary predispositions and cause mitochondrial disease. For example, there may be a link between pesticide exposure and the later onset of Parkinson's disease.
Other pathologies with aetiology involving mitochondrial dysfunction include schizophrenia, bipolar disorder, dementia, Alzheimer's disease, Parkinson's disease, epilepsy, stroke, cardiovascular disease, retinitis pigmentosa (eyes), and diabetes mellitus.
Mitochondria are sometimes said to have their own genome, often referred to as the "mitochondrial genome". Back to wikepedia for that one, but suffice to say the genome stored in the mitochondrial DNA if likened to a book would be about one billion words long, fascinating ain’t it? We are going to talk more on genomes and food as “Nutrigenomics” soon.
Labels: alzheimer's, antioxidants protect the mitochondria, bipolar, dementia, diabetes, dna, mitochondrial medicine, myopathy, oxidation, parkinson's