Life on Earth began about 4 billions years ago as single-cell organisms – bacteria and archaea - the 'prokaryotes', which lack a nucleus. The cyanobacteria (blue-green algae) were able to use the energy of the sun to combine carbon dioxide and water to produce simple carbohydrates, like glucose, and generated oxygen as the by-product.
About 2.4 - 2.2 million years ago, Earth experienced the Great Oxidative Event when there was a rapid rise in free oxygen generated by the photosynthetic action of cyanobacteria. This increase in atmospheric oxygen was toxic to many organisms and resulted in a mass extinction, but one of the beneficiaries was a new cell type called a ‘eukaryote’, which was formed from the union of an aerobic alphaproteobacterium and an archaeal cell. It was this new type of cell that enabled multicellular organisms, like plants and animals, to evolve for the first time. This critical event is known as the Endosymbiotic Theory of Evolution.
In this symbiotic relationship, the host archaeal cell provided protection and nutrients for the bacterium, which could use the now-abundant oxygen to produce energy to be used by itself and the host cell. Over time the bacterium evolved to become the specialized intracellular organelle called a mitochondrion, which is a tiny sausage-shaped structure, about 0.5–1-0 micron in diameter and 1–10 micron in length. Significantly, each partner of the union retained its own DNA. The cell’s nucleus contains two strands of DNA; in our case, one strand of DNA comes from our mother, and a complementary strand from our father. Located outside the nucleus, the mitochondrial DNA is inherited only from the mitochondria in our mother’s egg; the mitochondria in the fertilising sperm are destroyed. Mitochondrial DNA thus replicates entirely separately from the nuclear DNA, which means mitochondria can replicate themselves even when their host cell does not replicate.
Red blood cells apart, each eukaryote cell contains 1000 – 2000 mitochondria and they form the power plant of the cell. The mitochondria use oxygen to create the molecule ATP (adenosine triphosphate), which can be thought of as the unit of energy currency in all eukaryote cells. Research to understand how ATP is synthesized has led to several Nobel Prizes. The key enzyme involved, ATP synthase, is a membrane-bound protein that uses a proton-powered molecular rotor spinning at speeds of up to 21 000 rpm to synthesize ATP from ADP (adenosine diphosphate). The production of ATP depends on the voltage across the inner membranes of the mitochondrion. This membrane potential declines with age and disease, so reducing the amount of ATP produced. Reactive oxygen species also increase with reduced membrane potential and they induce oxidative stress, damage the mitochondrial DNA, and disrupt key reactions involved in the formation of ATP.
Mitochondria in the brain. This is a high-power electron microscope image of an ultrathin slice of a brain. The light-coloured structure containing multiple mitochondria, seen in cross-section, is part of the input region of a neuron, called a dendrite. Other mitochondria can be seen in the surrounding tissue. The multiple small circular structures seen near the synapse are synaptic vesicles, which contain small packages of neurotransmitter.
Electronmicrograph courtesy John Anderson
The large number of mitochondria contained in a single cell has been an essential factor in the success of decoding ‘fossil’ DNA, which is extracted from the skin or bones of extinct animals and our extinct hominid relations, like Neanderthals and Denisovans. Because the mitochondrial DNA has many copies per cell, while the nuclear DNA has only one pair, there is far more chance of recovering surviving fragments of mitochondrial DNA than of nuclear DNA. The mitochondrial DNA, which codes only for the organelle, is also very much shorter than the nuclear DNA, which has to code for the whole multicellular organism. This makes it far more likely that sufficient overlapping sequences of the fragments of mitochondrial DNA can be joined up to reconstruct a complete mitochondrial ‘genome’. By counting the similarities and mutations in the DNA of evolutionarily-related species is then possible to estimate when in pre-history the different species had a common ancestor – the ‘Mitochondrial Eve’.
LEDs come in variety of models.
So, what have Light Emitting Diodes (LEDs) got to do with mitochondria? The answer lies in the light-sensitive property of mitochondria. The membrane potential and ATP production is boosted when the mitochondria are exposed to light of near infrared wavelengths (700-1000nm), but the membrane potential is depressed by short wavelengths (420-450mn). And here’s the crunch: old-fashioned incandescent lights emit a broad spectrum of wavelengths (300-1400nm), whereas the dominant wavelengths in modern LED lights are typically much shorter (peaking around 450nm and no longer than 600nm) and this drives excessive production of reactive oxygen species that adversely affect the respiration of mitochondria. In contrast, long-wavelength light stimulates a key molecule (cytochrome C oxidase) in the chain of reactions that produce ATP.
In the absence of the boost by long wavelengths, the decline in mitochondrial has wide consequences and is implicated in a wide variety of pathologies, especially in tissues with high energy demand, like the retina. The production of reactive oxygen species in short wavelength light drives inflammation, cause cell death, and a decline of the organism. Is there a cure? In the case of the retina, Prof. Glen Jeffrey and colleagues at the Institute of Ophthalmology, UCL, found that visual sensitivity in humans working in LED-lit environments is improved when they are additionally exposed to infrared light.
Of course, LED lights are not the only modern introduction that impair mitochondrial function. Mitochondrial function is impaired by nutrient deficiencies as well as exposure to a long list of toxic metals and chemicals, including drugs like statins and antibiotics. Given the bacterial origins of mitochondria it is not surprising that antibiotics, which are designed to target bacteria, also damage mitochondria. And if you are a wannabee Captain James T. Kirk (or Major Tom) and want to boldly go where no man has gone before, then be aware that spaceflight is particularly stressful for mitochondria.
Not just humans, but other animals are subject to mitochondrial damage from environmental causes. Insecticides that contain neonicitinoids (‘neonics’) promote the production of reactive oxygen species that impair mitochondrial function. Neonics were widely used in agriculture, as they are taken up by the plant and had long-lasting toxic effects on the target predatory insects. They are now (finally) banned in the UK for agriculture, yet they remain widely used in veterinary products to control fleas and ticks. Neonics are water-soluble, so move freely into water courses, and may persist in the environment – in plants, soils and water - for months or even years. The primary reason for banning neonics in agriculture was because of the collateral damage they caused on so-called ‘non-target’ beneficial insects, particularly pollinators.
The primary action of the neonics is to over-stimulate neurotransmission at critical synapses, like the neuromuscular junction. (This over stimulation is effectively the insect equivalent of ‘lockjaw, which is caused by tetanus toxin). Not only insects are affected, however, bird nests incorporating cat and dog fur have been found to be contaminated with neonics, with dire consequences for the birds: unhatched eggs and dead chicks were more common in the nests with higher concentrations of neonics. Since virtually all our rivers are contaminated with neonics from agriculture and pet flea treatments, it is likely that our drinking water is also contaminated with low levels of neonics. Should we be worried? Probably, given the damage reactive oxygen species can wreak on mitochondria and other organs.
Is there any help for pollinators? Prof Glen Jeffrey and colleagues at UCL have found under laboratory conditions that the effects of neonics on honey bees are somewhat ameliorated by exposure to deep red light. Presumably bees foraging in the wild would be exposed to infrared sunlight and so gain some protection. Even so, neonics have been found to impair the navigation abilities of bumble bees and wild bees as they forage in the open. The solution, widely advocated, but yet to be legislated, is to ban all use of neonics, not just in agriculture, but in veterinary medicine too.
The possible health consequences of LED lighting on human mitochondria are now well-established, but are little-known outside scientific circles. The importance of regular exposure to infrared light needs to be more widely known, not just by the medical profession, but others like architects and developers who create our built environment. Those of us who are engaged in nature recovery projects can continue to swop all our incandescent lighting for LED lighting and sleep soundly, knowing that through our nature recovery activities our mitochondria will get a regular boost from exposure to infrared light.
Win-Win!
NRNers sowing the seeds of future biodiversity while bathing their mitochondria in infrared light.
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