They are incredibly small, kidney-shaped organelles that received almost no respect until the 1960s. It was during this time that Peter Mitchell developed the “chemiosmotic” proposal—demonstrating that energy was produced (in the form of ATP) by biological electron transfer within the mitochondrion of a cell. This work eventually earned Mitchell a Nobel Prize, and paved the way for future mitochondrial research. Stedman’s medical dictionary defines the mitochondrion as an organelle of the cell cytoplasm [i.e., outside the nucleus—BH] that is the principal energy source of the cell (McDonough, 1994, p. 629). In many biology classes, it is referred to as the “powerhouse” or “power plant” of the cell.
In an article titled “The Cost of Living,” biologist Peter Rich examined the effort and efficiency of mitochondria in a human at rest. In a detailed analysis of what these incredible organelles accomplish, he wrote:
An average human at rest has a power requirement of roughly 100 kilocalories (420 kilojoules) per hour, which is equivalent to a power requirement of 116 watts—slightly more than that of a standard household lightbulb. But, from a biochemical point of view, this requirement places a staggering power demand on our mitochondria. Mitchell’s work showed that the electrochemical gradient of protons across the inner mitochondrial membrane that drives ATP synthesis is roughly 200 mV, and most of this is the electric field component.
If it is assumed that 90% of human power is provided by the protons that are transferred through the ATP synthase, then the transmembrane proton flux would have to represent a current of 522 amps, or roughly 3 x 1021 protons per second.... Assuming a conversion efficiency that is close to unity [i.e., 100% efficiency], ATP is reformed at a rate of around 9 x 1020 molecules per second, equivalent to a turnover rate of ATP of 65 kg [143 lb.] per day and with much higher rates than this during periods of activity. This output is itself powered by the oxygen-consuming respiratory chain.
A typical adult male consumes around 380 litres of oxygen each day, and top athletes can sustain rates that are ten times greater for limited periods. Most (90%) of this oxygen is reduced to water by the terminal respiratory-chain enzyme, cytochrome oxidase. The inner mitochondrial membrane contains around 0.4 nanomoles of this enzyme per milligram of protein. It can work at a rate in excess of 300 electrons every second, but probably operates at an average rate of no more than 50 per second. Hence, an average human will need 2 x 1019 molecules [20 quintillion] of cytochrome oxidase to support oxygen consumption. With the inner mitochondrial membrane having a lipid/protein weight ratio of 1:1, the cytochrome oxidase would be associated with about 70 ml of lipoprotein membrane. However, the membrane’s thickness—only 6 nm [6 billionths of an inch]—means that the surface area of the inner mitochondrial membrane in an average human would be around 14,000 m2 (2003, 421:583, parenthetical items in orig., bracketed items and emp. added).
While you may not possess an in-depth knowledge of cytochrome oxidase or ATP synthesis, I think you would agree that the jobs carried out by mitochondria represent a Herculean task. In fact, Rich used those exact words, affirming: “This constant energy provision is a herculean task….” Indeed it is! However, instead of realizing the obvious—the ingenious design of this system—Rich looked at this Herculean task in a negative manner. He ended the above quote by stating: “This constant energy provision is a Herculean task, so it is not surprising that defects in mitochondrial function should lead to physiological disorders” (p. 583). He continued by speculating that things such as mitochondrial DNA mutations may contribute to “a reduced efficiency of energy provision.” In essence, rather than focusing on the incredible ability to power that “light bulb,” Rich was busy worrying about mutations that might eventually lead it to burn out.
Realizing just how much activity is going on “behind the scenes”—even while the human body is at rest—is awe-inspiring. These tiny organelles that are locked inside the cells of the body perform tasks that rival modern-day power stations. In his article, Rich noted: “The energy thus stored can be released by ATP hydrolysis, a reaction that is used by the myriad energy-requiring enzymes that maintain cellular function.” Humans possess a system capable of not only synthesizing energy from electrons derived from the food we eat, but also capable of storing and releasing this energy as it is needed. Additionally, we know that we can shower each day without the fear of receiving a shock or worrying about a short from this “internal power supply.” And yet, Rich felt compelled to attribute this “Herculean task” to mere chance. He noted:
It is generally accepted that the early and energetically inefficient eukaryotic cell was invaded more than a billion years ago by bacterium containing a much more efficient system for utilizing available energy sources—the oxygen-consuming respiratory chain. The majority of the bacterial genetic information was subsequently transferred to the nucleus, transforming the bacterial symbionts [an organism associated with another organism—BH] into slave mitochondrial organelles (p. 583).
What evidence exists for this theory? There is none!
Just for the sake of argument, if we were to assume that human cells received their mitochondria from bacteria millions of years ago, this still does nothing to explain how bacteria came to possess these astonishing organelles. Rocks and other nonliving material do not possess them. So how did these marvelous structures come into existence? We often hear the phrase, “He can’t see the forest for the trees.” This is just one more example of scientists detailing the extraordinary complexity and design of something, only to disregard the origin of that design and complexity, and then attribute it to mere happenstance.
Rich, Peter (2003), “The Cost of Living,” Nature, 421:583, February 6.
McDonough, James T. Jr., ed. (1994), Stedman’s Concise Medical Dictionary (Philadelphia: Williams & Wilkins), second edition.
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