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12. Life
| 12.23 |
A greater explanation of mitochondria and chloroplasts
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| Earlier, in section 12.7 (Life and the world of Solution Based Fusion) we discussed a key problem for early mono-cellular life being how to ensure the occurrence of key molecular reactions essential for providing food without destroying itself. | ||
| As we explained using the analogy of the car engine, cells also require the ability to source raw carbon, hydrogen, and other essential elements via strong chemical reactions in order to survive. The problem is the required internal reactions are simply too high for a single membrane cell to withstand such activities. | ||
| As our diagrams in Section 12.8 showed, Eukaryote cells (plants and animals) solved this challenge by incorporating co-dependent cells within themselves called mitochondria (plants and animals) and chloroplasts (plants only). In the diagrams, we described these as "Strong Chemical Fusion/Fission Engines". We will now discuss these most incredible of specialized"cells within cells" further. | ||
| 12.15.1 | A summary of chloroplasts | |
| Chloroplasts or "plastids" as they are also known are similar in many ways to mitochondria. They occur only in plants and photosynthetic eukaryotes and are the more ancient of the two co-dependent independent lifeforms that exist in cells. | ||
| Imagine again for a moment the incredible volatile conditions that represented the Earth two billion years ago. In a cruel twist, while the Earth's surface had cooled to enable life to sustain, ancient bacteria now face extinction from the lack of the very volatility of reactions that had helped it survive. | ||
| In an atmosphere full of carbon dioxide, sulphur and low of oxygen, a breed of bacteria adapted to the changing landscape by enveloping ancient chloroplasts to begin using sunlight and the atmospheric conditions to produce sufficient raw hydrogen, nitrogen and carbon for life- the process of photosynthesis. | ||
| Chloroplasts are the sites of photosynthesis in eukaryotes. They contain chlorophyll, the green pigment necessary for photosynthesis to occur, and associated accessory pigments ( caritenes and xanthophylls) in photo systems embedded in membranous sacs, thylakoids ( collectively a stack of thylakoids are a granum) floating in a fluid termed the stroma. | ||
| Like mitochondria, chloroplasts have their own DNA, termed cpDNA. Chloroplasts of Green Alea (protista) and plants ( descendents of some Green Algea) are thought to have originated by endosymbiosis of a prokaryotic algea, similar to to living Prochloron (prochlorobacteria). | ||
| In effect, oxygen is a by-product of the chloroplast reactions to produce simple food molecules capable of then being absorbed by cells containing chloroplasts. | ||
| 12.15.2 | A summary of mitochondria | |
| Every cell of an animal body contains many mitochondria. They produce most of the energis ( strong chemical fusion) and ergon transport fuel used by the body. Cells with a high metabolic rate (heart muscle cells) may contain many thousands of mitochondria. Some cells may contain only dozens. | ||
| Mitochondria convert energy found in nutrient molecules and store it in the form of adenosine triphosphate (ATP). ATP is the universal energis-yielding commodity in cells, used by enzymes to perform a wide range of cellular functions. We cannot survive, even for a moment, without a sufficient supply of ATP. | ||
| Mitochondrial energis production is a foundation for health and well being. It is necessary for physical strength, stamina and consciousness. Even subtle deficits in mitochondrial function can cause weakness, fatigue and cognitive difficulties. Chemicals which strongly interfere with mitochondrial function are known to be potent poisons. During aging, mitochondrial function may become compromised. | ||
| Mitochondria vary considerably in shape and size, but all have the same basic architecture. There is a smooth outer membrane, surrounding a very convoluted inner membrane. The convolutions form recognizable structures called cristae. The two membranes have very different properties. Together they create two compartments, namely the inter membrane space (the compartment between the membranes), and the matrix (the very interior of the mitochondria). | ||
| 12.14.3 | The mitochondria energis/ergon cycle | |
| In order to carry out energy conversion, mitochondria require oxygen, which they convert to water. The purpose of our respiratory and circulatory systems is to deliver oxygen to the tissues for use by mitochondria, and to eliminate carbon dioxide. The consumption of oxygen by mitochondria is called cellular respiration. | ||
| Mitochondrial energis production is accomplished by two closely linked metabolic processes. | ||
| (a) HAPPY DIGESTION-First, the citric acid cycle converts biological fuel (carbohydrates and fatty acids) into ATP (adenosine triphosphate) and hydrogen (in the form of NADH and FADH2) | ||
| 2) DEEP, SLOW BREATHING- Second, the electron transport chain combines hydrogen with oxygen to generate abundant ATP in a highly efficient and tightly controlled manner. | ||
| Mitochondrial efficiency has been reported to be close to 70%, which compares quite favorably with internal combustion engines (about 10% efficient) or hydrogen-oxygen fuel cells used in spacecraft (approximately 40% efficient). | ||
| The process of generating ATP with oxygen is called oxidative phosphorylation. This process generates approximately ten times more ATP than the citric acid cycle alone, and generates more ATP than any other energy-producing pathway (e.g., glycolysis). Oxidative phosphorylation is the primary energy process for all aerobic organisms. | ||
| 12.15.3 | Mitochondria have their own DNA | |
| One interesting property of mitochondria is that they have their own DNA. Mitochondrial DNA (mtDNA) is the same as ancient bacteria in that it exists as a simple loop. That Mitochondria have their own DNA is a living fact to their origin as independent bacteria and their function as individual organisms co-operating within a cell environment. | ||
| 12.15.4 | The importance of Mitochondria and ageing | |
| While animal DNA has a number of functions that ensure replication and protection of the code is maintained, Mitochondria does not. For example, mtDNA does not have the protective sheaths (histones) that DNA has. Nor does mtDNA have the self repair mechanisms that animal cells have. | ||
| What this means is that over time, it has been estimated the relatively unprotected and un repaired mtDNA suffers more than ten times the damage that nuclear DNA does This leads to mitochondrial dysfunction, disruption of cellular energy production, and accelerated cellular aging. | ||
| Mitochondrial electron transport is not perfect. Even under ideal conditions, some electrons leak from the electron transport chain. These leaking electrons interact with oxygen to produce super oxide radicals. With mitochondrial dysfunction, leakage of electrons can increase significantly. The close proximity of mtDNA to the flux of super oxide radicals (or hydroxyl radicals), and it is the lack of protection and repair mechanisms, leads to free radical-mediated mutations and deletions. Mitochondrial aging has been proposed as an underlying cause of 1) free-radical stress, 2) degenerative disease and 3) aging. | ||
| Evidence is accumulating that mitochondrial dysfunction underlies many common pathologies. Mitochondrial defects have been identified in Parkinson's disease, Alzheimer's disease, heart disease, fatigue syndromes, numerous genetic conditions, and nucleoside therapy for AIDS. Also, many common nutritional deficiencies can impair mitochondrial efficiency. | ||
| One of the mitochondrial components which may play a critical role in the aging of mitochondria is cardiolipin (diphosphatidylglycerol), a special phospholipid that is unique to the inner mitochondrial membrane and which provides important structural support to several of the enzymes in the electron transport chain Carnitine is necessary to transport long-chain fatty acids into the mitochondrion for use as fuel and for the manufacture of cardiolipin. Medium- and short-chain fatty acids less than 8 carbons in length do not require carnitine transport. | ||
| Cardiolipin levels decrease with age, as does mitochondrial efficiency. Acetyl-L-carnitine (ALC) restores falling cardiolipin levels in aged rat mitochondria to youthful levels. | ||
| ALC treatment also restores ADP carrier activity and cytochrome oxidase activity. Since the amounts of cytochrome protein and ADP carrier protein in aged mitochondria is close to that in young mitochondria, it is the enzyme efficiencies which are being adversely affected by aging influences - and restored by ALC administration. ALC has no effect on cytochrome oxidase activity in young rat mitochondria. | ||
| By restoration of cardiolipin levels, cytochrome oxidase activity and ADP carrier transport, ALC also restores overall respiratory activity (oxygen energy conversion) of aged rat mitochondria to normal levels. We believe it may help normalize human mitochondrial function as well. | ||
| Coenzyme Q | ||
| Coenzyme Q (ubiquinone) is a critical electron transfer molecule that transports electrons from Complexes I and II to Complex III. It is present in much higher amounts than the complex proteins and is probably mobile within the membrane. It can exist in reduced (quinol) and oxidized (quinone) forms, as well as an intermediate radical form (a semiquinone radical). Deficiencies of coenzyme Q are associated with numerous pathologies, the most common of which is probably cardiomyopathy (heart muscle disease). The heart muscle is especially rich in mitochondria due to its extremely high energy requirements. It is no accident that cardiolipin was first extracted from heart muscle mitochondria. | ||
| Coenzyme 1 | ||
| NADH (also called coenzyme 1) is a key electron transfer molecule between the citric acid cycle and Complex I. NAD (short for nicotinamide adenine dinucleotide) exists in both oxidized (NAD+) and reduced (NADH) forms. Both forms participate in countless reactions throughout the body, where NAD+ serves as an electron acceptor and NADH as an electron donor. The electron transport chain starts with NADH on Complex I and ends with oxygen on Complex. | ||
| Although the mechanism of inhibition of Complex I in Parkinson's disease is not known, NADH supplementation has demonstrated clinical value in treating Parkinson's disease. Under average circumstances, about one-third of NAD is produced from vitamin B3 (niacin or niacinamide) and about two-thirds from the catabolism of tryptophan. | ||
| Lipoic Acid | ||
| Lipoic acid (lipoate) is an essential component of the alpha-ketoglutarate dehydrogenase complex (KGDHC), the closely associated collection of enzymes that generates NADH from the decarboxylation of alpha-ketoglutarate within the citric acid cycle. Also called thioctic acid, lipoate exists in both oxidized (disulfide) and reduced (dithiol) forms. Thiamine diphosphate (a vitamin B1 derivative) and FAD (a riboflavin derivative) are also cofactors of KGDHC. | ||
| Lipoate, thiamine diphosphate and FAD also serve as a cofactors in the pyruvate dehydrogenase complex, an enzyme complex quite similar to KGDHC in both structure and function. Like KGDHC, the pyruvate dehydrogenase complex generates NADH. While KGDHC generates succinyl-CoA within the citric acid cycle, pyruvate dehydrogenase complex generates acetyl-CoA that feeds the citric acid cycle. Specifically, acetyl-CoA is a substrate for citrate synthase to generate citric acid (citrate) at the start of the citric acid cycle. | ||
| Of all of the enzymes of the citric acid cycle, only the KGDHC and citrate synthase catalyze directional reactions. All of the other reactions are reversible (they can run forwards and backwards, illustrated by double-headed arrows). Both of these directional or driving reactions force the citric acid cycle to flow in the correct direction, the direction that generates NADH, FADH2 and ATP. Both of these directional reactions require the involvement of dehydrogenase complexes which are dependent on lipoic acid and vitamins B1 and B2 for their activity. In addition to it's cofactor role, lipoic acid is a powerful antioxidant that is effective at scavenging both water- and lipid-soluble free It picks up some of the free radicals that vitamin C and E miss. Lipoate decreases the excitotoxicity of glutamate and is used to treat diabetic polyneuropathy | ||
| Supplementation | ||
| There is plenty of evidence that documents the potential effectiveness of diet and dietary supplements on the mitochondrial pathologies underlying Parkinson's disease and aging. Not only do numerous nutrients play indispensable roles in mitochondrial energy function, nutrients also serve vital antioxidant functions that ameliorate the free-radical byproducts of oxidative phosphorylation. In aged rats and mice, antioxidant supplements of vitamins C and E, and the amino acid cysteine, are effective in 1) lowering the amount of oxidized glutathione and 2) reducing DNA damage. Untreated, old rodents have several times more oxidized glutathione in their livers and up to six times more oxidized glutathione in their brains. Such changes reflect the general increase in oxidative stress that occurs with age and a gradual decrease in the competence of the antioxidant defense system. One obvious mitochondrial component of this defense is the production of reduced NADH, FADH2 and NADPH which can directly reduce (recycle) oxidized substrates into their reduced forms. | ||
| Although antioxidant therapy is an obvious approach to deal with increased oxidative stress and decreased antioxidant levels, scientists and doctors have been slow to apply this technology. Researchers have started investigating the effect of vitamin E towards this end, but antioxidants are much more effective in combinations than they are singly. More importantly, vitamin E is lipid soluble and provides minimal antioxidant protection to the aqueous (watery) metabolic compartments of the brain that are stressed in Parkinson's disease. It makes much better sense to employ a broad-spectrum antioxidant intervention which emphasizes water-soluble antioxidants like vitamin C, glutathione, N-acetylcysteine, polyphenols, proanthocyanidins, lipoate, NADH, DMSO, etc. This general approach has been pioneered by Annetta Freeman with outstanding results. | ||
| Cognitive Enhancement | ||
| At this time, the degree of mitochondrial involvement in age-related mental decline (ARMD) and age-associated memory impairment (AAMI) is not known. A significant amount of the mitochondrial DNA (mtDNA) damage seen in Parkinson's disease is also observed in age-matched controls. Such observations suggest that reductions in mitochondrial efficiency and ATP output may underlie many age-associated phenomena. The successful use of mitochondrial support nutrients to ameliorate serious mitochondrial diseases may prove to be generalized to the sub clinical complaints of normal, healthy, aging humans. | ||
| 12.15.5 | The missing understanding of original motion and mitochondria- chloroplasts | |
| Something that is often missed in investigations into the function of cells is the fact that everything is in motion in some way. The natural assumption about motion is that it is there because of operations within the organism. But what of the origin of cellular motion? At what point of origin does motion originate? | ||
| The strong chemical reaction that occurs within the "bellows" structure of the mitochondria is the same (but smaller) as that which occurs in a car engine. The strong structure of the cylinder and engine block means the mini-explosion of motion is directed upwards push the cylinder head. What then do you think happens to the "bellows" structure of the mitochondria at such a point? | ||
| As you may have guessed, the shape of the mitochondria expands rapidly, causing a ripple effect of motion throughout the cell. Depending on where the reaction occurs, the main wavefront of motion can be directed- directed motion, such as towards the nucleus, or a component within the cell that needs to be moved. | ||
| Without directed motion, cells could not function. The existence of directed motion represents a fundamental tenet of intelligence we call "volition"- willful movement. | ||
| More than just the chemical conversion within mitochondria and chloroplasts, it is the motion created by those chemical reactions that are fundamental to the survival of eukaryote (plant and animal) cells. | ||
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