Why does cell division, as asexual reproduction, perpetuate life of unicellulars - (Jan/02/2019 )

Hi everybody.
I am an IT developer, not a biologist, so thank you for going extra to provide explanations for what I do not have from formal education.

Let me add more details to the title so it has more meaning:
 

Well, the mass is not conserved - your own cells are not made up of the exact same components today as they were a few years ago. Cells constantly produce waste via a number of processes, and take up (and release) a wide variety of substances. This is why we need to ingest food on a regular basis - it provides the energy for the chemical reactions and substrates for metabolism and division, repair, etc of the cells.The same applies to single-celled organisms - they metabolize nutrients to produce waste products and repair and replicate the cell.  The division process is not equal either - the daughter cells are made up of 50% or less of the parent, then add mass by ingesting nutrients. the so-called immortality of single cell organisms (and some multicellular too) is a bit of a misnomer: there are two types of division here - asymmetric and symmetric. In the asymmetric, only the daughter cell is "refreshed", in the symmetric (also called binary fission ), both are "refreshed", but I am not sure that the exact mechanisms for this are known.

Free radicals are very short lived in real-life, they are highly reactive and are actively scavenged by a number of substances produced by most (I don't know about all) organisms - a common scavenger is (hydrogen) peroxide. These do not accumulate in the cells to any degree. Mutations in DNA induced by radiation and free-radical reactions can be repaired by cellular mechanisms in most instances, and those that do accumulate are not guaranteed to cause a deleterious effect or to be in a region that codes for a protein. There is also redundancy in coding for most amino-acids, and usually some flexibility in which amino-acid can occupy which position in the protein (look at the charge properties and structures of the amino acids). In many instances there is also redundancy for proteins - several proteins are coded that can perform the same function. Those mutations that are deleterious might not have a significant effect on the organism - perhaps it takes a little longer to process a metabolite. 

It should also be noted that the DNA replication process is not perfect either, it's very very good, but each replication cycle will result in a few base pair changes over a genome - the same as might result from radiation etc. 

Serious damage to the cell results in death of the cell - ever had a sunburn? The dry flaky skin that sloughs off is the cells that didn't manage to repair the damage - the ones that did survive might have accumulated mutations, some of which can lead to cancers (e.g. melanoma). In the case of unicellular organisms, the individual cell will die, or potentially be selected against in the environment (if the mutation causes a significant deleterious effect).

You must remember that for any group of organisms, there is a range (bell curve/normal distribution) of conditions in which they will be fit, and some will be "more fit" than others -better suited to the conditions in which they grow, and so will reproduce more/faster etc and in theory dominate the population to become "more fit" over time (narrower bell curve). However this isn't the full story - each generation of those cells will contain mutations that are capable of being selected for and against, shifting the bell curve peak to the left or right. So this accumulation of mutations is actually a good thing for a species overall, as it allows adaptation to new conditions over time.

Hi Bob.
 

You answer contains lots of useful information, I did some reading after it.

But is it really answering the original question - " why would single cell that does not divide die, while cell division and replication leads to life continuation? " ?

The only direct reference in your answer is in the sentence:

both are "refreshed", but I am not sure that the exact mechanisms for this are known."
which to me seems like putting a massive question mark on our knowledge of the actual mechanism that facilitate life extension, next to all that we know.

I am also struggling to understand the main tendency in your answer - I see it focuses on negating the contribution of the death causes listed above, but I am not sure about the ending conclusion (as death exists for sure  )

Thank you for answering

I answer as I did because the mechanisms are not known, at least to my knowledge, which is limited as I do not work on these areas at all. 

A single cell dies because of the accumulation of damage from all sorts of things over time - we don't fully know the triggers for this as it is multi-factorial and will depend on the environment in which the cell exists. We also (as far as I know) don't fully know why cells can regenerate when they replicate, other than that the cell can at least partially repair faults in its DNA during the replication process. We also don't fully know why some cells from multicellular organisms are terminally differentiated and will not divide again once they reach that state (e.g. neurons).

Death certainly exists for cells, in many different forms, and there are even forms that are terminal but not death (e.g. senescence),  and the triggers for each different type of cell death are not fully understood (again, as far as I know - I'm not studying this area). We understand that under certain conditions some forms of cell death are activated and we even know some of the mechanisms, but even the most simple bacterial cell encodes thousands of proteins many of which we don't even know the function of yet. 

As a simple system take norovirus. A small non-enveloped protein with a genome of about 7500 bases - this encodes 8 known proteins. We still don't know the full range of functions of each of these proteins, and how they interact with cellular systems. As a more complex system - look at a very very well known protein - p53, which is associated with a large number of cancers and we have been studying for nearly 40 years (since 1979) - we are still finding interactions and systems in which it plays a role (including apoptosis, one of the cell death pathways).

I answer this way to help you understand that biological systems are very very complex and we are only just starting to have the tools to analyze and understand multi-component systems, and as yet our understanding is limited -we are constantly finding new functions for things we thought we knew well (e.g. RNA, where it has been realized in the past 10-15 years that there are many more forms of RNA (mRNA, cRNA, miRNA, shRNA, siRNA, chemically modified: methylations (5 different types), glycosylations, etc...) than we realize and each has an independent role dependent on the system it is interacting with).

Thanks for the comprehensive answer