Mitochondria are the cell’s power producers. They convert energy into forms that are usable by the cell. Located in the cytoplasm, they are the sites of cellular respiration which ultimately generates fuel for the cell’s activities. Mitochondria are also involved in other cell processes such as cell division and growth, as well as cell death. They convert oxygen and nutrients into adenosine triphosphate (ATP). ATP is the chemical energy “currency” of the cell that powers the cell’s metabolic activities. This process is called aerobic respiration and is the reason animals breathe oxygen.
Mitochondria are bounded by a double membrane. Each of these membranes is a phospholipid bilayer with embedded proteins. The outermost membrane is smooth while the inner membrane has many folds. These folds are called cristae. The folds enhance the “productivity” of cellular respiration by increasing the available surface area. The double membranes divide the mitochondrion into two distinct parts: the intermembrane space and the mitochondrial matrix. The intermembrane space is the narrow part between the two membranes while the mitochondrial matrix is the part enclosed by the innermost membrane.
Several of the steps in cellular respiration occur in the matrix due to its high concentration of enzymes. Mitochondria are semi-autonomous in that they are only partially dependent on the cell to replicate and grow. They have their own DNA, ribosomes and can make their own proteins. Similar to bacteria, mitochondria have circular DNA and replicate by a reproductive process called fission. The inner membrane selects over what materials are allowed through it and it is known that active transport mechanisms involving translocase enzymes are responsible for the movement of ADP and ATP across it.
Mitochondria use respiration to brake down high energy molecules such as sugars and store that energy as ATP (produced from ADP & a phosphate) The raw materials used to generate ATP are the foods that we eat, or tissues within the body that are broken down in a process called catabolism. The breaking down of food into simpler molecules such as carbohydrates, fats, and protein is called metabolism. These molecules are then transferred into the mitochondria, where further processing occurs.
The reactions within the mitochondria produce specific molecules that can have their electrical charges separated within the inner mitochondrial membrane. These charged molecules are processed within the five electron transport chain complexes to finally combine with oxygen to make ATP. The process of the charged substances combining with oxygen is called oxidation, while the chemical reaction making ATP is called phosphorylation. The overall process is called oxidative phosphorylation. The product produced by this process is ATP. Using Oxygen to Release Energy
Mitochondria are used in cellular respiration. The matrix is filled with water and proteins (enzymes). Those proteins take food molecules and combine them with oxygen. 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. On the ethical implications of mitochondrial DNA analysis: Mitochondrial DNA analysis is a somewhat different type of DNA analysis compared to other techniques used today.
It generally works well on samples that are unable to be analysed through numerous other techniques. So is There a Risk From Complete mtDNA Sequencing ? Yes, and the risk from having a complete mtDNA sequencing begins when a person first thinks about ordering the test – as for the first time it is possible to have a test performed for genealogical purposes that can actually affect the person’s well being. Before agreeing to mtDNA sequencing it is important to consider just how one might be affected by the results.
Fortunately, for about 90-95% of people the results will not show any mutations of medical significance. But this means that about 5-10% of people can expect results that show a significant mutation—for example, as is shown in Table 12 where the subject has the significant mutation at A4295G. Because of the random nature of mutations, it is impossible to predict in advance who might receive such results. The figure of 5-10% is the present author’s estimate from studying the mutations found in all of the 2,500 published complete mtDNA sequences.
It is possible that some of the sequences have been published by the researchers because of the mutations that the sequences contain—this would make the 5-10% figure too high. But against this, mutations associated with medical conditions continue to be identified—this would raise the figure. The author suggests the figure of 5-10% when mtDNA is sequenced for genealogical purposes. Besides the person themselves worrying, should they be telling other people that they are going to be tested? And, if so, who should be told? Close relatives and doctors, perhaps.
But probably not at this early stage an employer or health insurance company. It is difficult to judge how important pre-testing anxietymight become, but for some people, fear of adverse results will quite properly stop them from undergoing the testing. However, if mtDNA sequencing is undertaken it becomes important to determine just how significant the results might be. The results for the Haplogroup H9 person shown earlier, demonstrate that test results can suggest there are no adverse medical mutations, and in such a case there would not appear to be any reason for concern.
For the great majority of tests the outcome will be similar. But what about a case such as that for the Haplogroup K1 person (shown earlier)? Here the results suggest that the subject has a mutation linked to a significant heart condition. In such a situation it would seem important to convey things in their proper proportions and give the person the most complete understanding of the situation as is possible. In most instances it would be sufficient to explain that most mtDNA mutations do not cause the disease with which they are associated, but rather explain why the particular condition might arise.
Just at present it would seem that most genealogical testing companies are not involving themselves in analysing their results for any medical implications; and it is uncertain how such service might be provided. But what is clear is that counselling people who have been been found to have important mutations will not be easy, and perhaps will lead to as many unanswerable questions being posed, as questions for which answers can be given. But it is not just the person who receives test results indicating possible medical problems who is affected—other family members will also have obvious concerns.
A mother who receives adverse test results will certainly worry about the health of her children; and a younger person will have concerns about their siblings and mother. Medically significant mtDNA mutations should not be ignored, in the author’s view, and their possible significance should be discussed with the family’s medical practitioners. Overall, the discovery of potentially harmful mtDNA mutations may have many unexpected and undesirable consequences. Given the role of mitochondria as the cell’s powerhouse, there may be some leakage of the high-energy electrons in the respiratory chain to form reactive oxygen species.
This can result in significantoxidative stress in the mitochondria with high mutation rates of mitochondrial DNA. A vicious cycle is thought to occur, as oxidative stress leads to mitochondrial DNA mutations, which can lead to enzymatic abnormalities and further oxidative stress. A number of changes occur to mitochondria during the aging process. Tissues from elderly patients show a decrease in enzymatic activity of the proteins of the respiratory chain. Large deletions in the mitochondrial genome can lead to high levels of oxidative stress and neuronal death in Parkinson’s disease.
Hypothesized links between aging and oxidative stress are not new and were proposed over 50 years ago however, there is much debate over whether mitochondrial changes are causes of aging or merely characteristics of aging. One notable study in mice demonstrated shortened lifespan but no increase in reactive oxygen species despite increasing mitochondrial DNA mutations, suggesting that mitochondrial DNA mutations can cause lifespan shortening by other mechanisms. As a result, the exact relationships between mitochondria, oxidative stress, and aging have not yet been settled.
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