So a cell always has functional mitochondria. The mitochondria multiply within a cell (and their DNA is replicated), while the cell grows between divisions.
Nevertheless, not all ATP is produced by the mitochondria. For example ATP is produced by various chemical reactions that do not need dioxygen (i.e. which also work during anaerobic effort or whenever the power requirements exceed the maximum output of the mitochondria), e.g. by the hydrolysis of phosphocreatine (vertebrates) or of phosphoarginine (arthropods), or by the splitting of glucose into lactic acid.
So a cell can survive for some time without mitochondria, but it will exhaust quickly all its energy reserves.
Also if you really want an intellectual challenge and to help me on a problem I fail to understand, is the debate on mildronate vs ALCAR effect on health. Mildronate: The main cardioprotective effects of meldonium are mediated by the inhibition of GBB. By subsequently inhibiting carnitine biosynthesis, fatty acid transport is reduced and the accumulation of cytotoxic intermediate products of fatty acid beta-oxidation in ischemic tissues to produce energy is prevented, therefore blocking this highly oxygen-consuming process.[4] Treatment with meldonium therefore shifts the myocardial energy metabolism from fatty acid oxidation to the more favorable oxidation of glucose, or glycolysis, under conditions where oxygen is limited. It also reduces the formation of trimethylamine N-oxide (TMAO), a product of carnitine breakdown that has been implicated in the pathogenesis of atherosclerosis and congestive heart failure. https://en.wikipedia.org/wiki/Meldonium#Physio-pharmacology
https://en.wikipedia.org/wiki/Acetylcarnitine#Biochemical_pr... ALCAR has many many studies showing a potent improvement of health/metabolism and especially a reduction of oxidative stress. Despite this, ALCAR supposedly do the opposite of mildronate, it shift the mitochondria bioenergetics to an increase in beta oxidation and reduce glucose consumption. Beta oxidation is oxidative stress but I believed glucose oxidation leads to more oxidative stress?
How to make sense of those contradicting both positive narratives ?? Also weird detail: Excess acetyl-CoA causes more carbohydrates to be used for energy at the expense of fatty acids. This occurs by different mechanisms inside and outside the mitochondria. ALCAR transport decreases acetyl-CoA inside the mitochondria, but increases it outside.[4][5] plz halp
ATP is a highly unstable molecule, precisely due to its high energy content. It cannot be effectively supplemented exogenously.
[1] - https://www.youtube.com/watch?v=06e-PwhmSq8 [video]
As for cell division, the simplest and maybe partial but best explanation would be that prior to cell cloning, the cell induce mitochondria cloning proactively. Therefore it would have excess mitochondria in order to havz them already ready for the cloning stage.
My limited understanding is that can is the key word. There are apparently factors that can lead to the cell switching from OxFox to the primitive method of ATP generation which may actually be the original default state of operation for the cell prior to mitochondria being introduced. This may be an early state that existed prior to there being much O2 in the atmosphere when lifeforms were much more primitive. Again, this is not my area of expertise and I am not sure that scientists fully understand this yet either.
> "The ‘reverse’ Krebs cycle was first proposed in 1966. It does exactly the opposite; it uses energy to react the gases hydrogen and carbon dioxide to make Krebs-cycle intermediates, turning simple gases into the molecules of life. The bacteria that live this way are a billion years older than the first photosynthetic cyanobacteria and thrive in environments where life might have started, such as hydrothermal vents."
https://www.ukri.org/blog/understanding-the-origins-of-life-...