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unbreakable DNA


fredreload

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Keep in mind that DNA damage and DNA mutation are two different things when you are reading this post.

 

So here I start another post based on jimmydasaint's request. The question revolves around DNA damage and aging again. About my speculation in simple term, when I was born my DNA is perfect with no DNA damage of aging because I start out as normal born baby. Now as time goes on my DNA starts to get lesions, not mutations, as I grow old, that's what the DNA damage theory says. Now this theory does not go into replication but I speculate that when I am 30 years old and my cell goes through mitosis, it produces an identical 30 years old cell, not baby cell, equally damaged because it is old. Speculation continues, now at age 30 I produce sperm and if I get lucky I would get a female mate of 28 and have a baby. Now the baby is not of age (30+28)/2=29 years old when it's born, the baby also doesn't age faster normally. This could only mean that the sperm and ovum cell's DNA does not have any lesions because the baby has a perfect DNA. The sperm is produced from the testes germ cells through mitosis. Now here's the important speculation part of two points for myself at 30 years old.

 

1. The DNA of the germ cells in the testes is a fresh copy ever since I am born. It remains the same and does not receive any lesions that would cause it to age.

2. The DNA of the germ cells also receive lesions and ages, but in meiosis I and meiosis II and become zygote and eventually baby have an important step that fixes these lesions with a perfect repair, not the usual partial repair we have in our cells, it could also be that the genes are shuffled around in meiosis I and meiosis II that fixes the damage.

 

Why do I come to this conclusion? Because the baby is not of age 29 years old when it's born or the baby ages faster with a damaged DNA, the baby's DNA has to be perfect with no damages when it's born.

Now for the conclusions for speculations 1 and 2:

 

1. For speculation 1, if we can obtain an undamaged DNA from the germ cells then we know which part of the DNA is damaged in other cells of the body and attempt to replace them with the undamaged one assuming all the DNA in our body are the same but only differs with gene expression.

2. For speculation 2, we need to identify the step that does a perfect repair to the DNA and duplicate that process for all the cells in our body.

Keep in mind that in order to change the DNA in our body we need a nanomachine, crispr also works but we need 100% accuracy. I haven't found a DNA nanomachine capable of altering DNA.

 

P.S. I feel that the DNA damage theory is a bit outdated, everyone follow a set age normally of 100+- years of age. You don't live longer or shorter because of damages done to your DNA

 

For a short chart:

1. parent undamaged DNA + parent undamaged DNA -> baby undamaged DNA

2. perfect repair(parent damaged DNA) + perfect repair(parent damaged DNA) -> baby undamaged DNA

Edited by fredreload
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Keep in mind that DNA damage and DNA mutation are two different things when you are reading this post.

 

So here I start another post based on jimmydasaint's request. The question revolves around DNA damage and aging again. About my speculation in simple term, when I was born my DNA is perfect with no DNA damage of aging because I start out as normal born baby. Now as time goes on my DNA starts to get lesions, not mutations, as I grow old, that's what the DNA damage theory says. Now this theory does not go into replication but I speculate that when I am 30 years old and my cell goes through mitosis, it produces an identical 30 years old cell, not baby cell, equally damaged because it is old. Speculation continues, now at age 30 I produce sperm and if I get lucky I would get a female mate of 28 and have a baby. Now the baby is not of age (30+28)/2=29 years old when it's born, the baby also doesn't age faster normally. This could only mean that the sperm and ovum cell's DNA does not have any lesions because the baby has a perfect DNA. The sperm is produced from the testes germ cells through mitosis. Now here's the important speculation part of two points for myself at 30 years old.

 

1. The DNA of the germ cells in the testes is a fresh copy ever since I am born. It remains the same and does not receive any lesions that would cause it to age.

 

I disagree here. Germ cell DNA is at least as sensitiive to lesions or mutagenesis as body cells. In fact DNA damage to sperm DNA can cause infertility. In addition, Reactive Oxygen Species (ROS) may damage oocytes, but that is a speculation.

 

 

 

DNA damage in sperm is one of the major causes of male infertility and is of much concern in relation to the paternal transmission of mutations and cancer (Zenzes, 2000; Aitken et al., 2003; Fernández-Gonzalez, 2008). It is now clear that DNA damaged spermatozoa are able to reach the fertilization site in vivo (Zenzes et al., 1999), fertilize oocytes and generate early embryos both in vivo and in vitro. The effect of ROS on human oocytes is not as easy to study or quantify. It is a common consensus that the maternal genome is relatively well protected while in the maturing follicle; however damage may occur during the long quiescent period before meiotic re-activation (Zenzes et al., 1998). In fact, during the final stages of follicular growth, the oocyte may be susceptible to damage by ROS.

 

http://www.ncbi.nlm.nih.gov/pubmed/20663262

 

2. The DNA of the germ cells also receive lesions and ages, but in meiosis I and meiosis II and become zygote and eventually baby have an important step that fixes these lesions with a perfect repair, not the usual partial repair we have in our cells, it could also be that the genes are shuffled around in meiosis I and meiosis II that fixes the damage.

 

Why do I come to this conclusion? Because the baby is not of age 29 years old when it's born or the baby ages faster with a damaged DNA, the baby's DNA has to be perfect with no damages when it's born.

 

I don't know about meiotic repair, you would have to cite something to prove your point. Nevertheless, repair mechanisms occur to re-age chromatin in germ cells:

 

 

 

Telomeres protect and cap linear chromosome ends, yet these genomic buffers erode over an organism’s lifespan. Short telomeres have been associated with many age-related conditions in humans, and genetic mutations resulting in short telomeres in humans manifest as syndromes of precocious aging. In women, telomere length limits a fertilized egg’s capacity to develop into a healthy embryo. Thus, telomere length must be reset with each subsequent generation. Although telomerase is purportedly responsible for restoring telomere DNA, recent studies have elucidated the role of alternative telomeres lengthening mechanisms in the reprogramming of early embryos and stem cells, which we review here.

 

http://www.hindawi.com/journals/bmri/2014/925121/

 

 

Now for the conclusions for speculations 1 and 2:

 

1. For speculation 1, if we can obtain an undamaged DNA from the germ cells then we know which part of the DNA is damaged in other cells of the body and attempt to replace them with the undamaged one assuming all the DNA in our body are the same but only differs with gene expression.

2. For speculation 2, we need to identify the step that does a perfect repair to the DNA and duplicate that process for all the cells in our body.

Keep in mind that in order to change the DNA in our body we need a nanomachine, crispr also works but we need 100% accuracy. I haven't found a DNA nanomachine capable of altering DNA.

 

I thought that different humans would receive different damage depending on exposure to different ROS, different chemicals (mutagenesis), different diet, different ages (older people accumulating more hypothesised damage, different genders, different professions etc... I think you would struggle to ask 100 women to donate their ova and for your research to be performed unless the legislative authorities allow experiments on human eggs. There is a serious ethical issue here, in my opinion, which religious groups would jump upon. As for nanomachines, I don't imagine that nanoscience has yet reached this stage.

 

P.S. I feel that the DNA damage theory is a bit outdated, everyone follow a set age normally of 100+- years of age. You don't live longer or shorter because of damages done to your DNA

 

For a short chart:

1. parent undamaged DNA + parent undamaged DNA -> baby undamaged DNA

2. perfect repair(parent damaged DNA) + perfect repair(parent damaged DNA) -> baby undamaged DNA

 

How many sperm would be repaired given that there are 300 million approx. released per ejaculation?

 

The idea is good and you posted in the correct place. But, it needs a bit more background research about what is possible and what is not yet in the vista of scientific capability.

Edited by jimmydasaint
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Keep in mind that DNA damage and DNA mutation are two different things when you are reading this post.

 

So here I start another post based on jimmydasaint's request. The question revolves around DNA damage and aging again. About my speculation in simple term, when I was born my DNA is perfect with no DNA damage of aging because I start out as normal born baby. Now as time goes on my DNA starts to get lesions, not mutations, as I grow old, that's what the DNA damage theory says. Now this theory does not go into replication but I speculate that when I am 30 years old and my cell goes through mitosis, it produces an identical 30 years old cell, not baby cell, equally damaged because it is old. Speculation continues, now at age 30 I produce sperm and if I get lucky I would get a female mate of 28 and have a baby. Now the baby is not of age (30+28)/2=29 years old when it's born, the baby also doesn't age faster normally. This could only mean that the sperm and ovum cell's DNA does not have any lesions because the baby has a perfect DNA. The sperm is produced from the testes germ cells through mitosis. Now here's the important speculation part of two points for myself at 30 years old.

 

1. The DNA of the germ cells in the testes is a fresh copy ever since I am born. It remains the same and does not receive any lesions that would cause it to age.

 

I disagree here. Germ cell DNA is at least as sensitiive to lesions or mutagenesis as body cells. In fact DNA damage to sperm DNA can cause infertility. In addition, Reactive Oxygen Species (ROS) may damage oocytes, but that is a speculation.

 

 

 

DNA damage in sperm is one of the major causes of male infertility and is of much concern in relation to the paternal transmission of mutations and cancer (Zenzes, 2000; Aitken et al., 2003; Fernández-Gonzalez, 2008). It is now clear that DNA damaged spermatozoa are able to reach the fertilization site in vivo (Zenzes et al., 1999), fertilize oocytes and generate early embryos both in vivo and in vitro. The effect of ROS on human oocytes is not as easy to study or quantify. It is a common consensus that the maternal genome is relatively well protected while in the maturing follicle; however damage may occur during the long quiescent period before meiotic re-activation (Zenzes et al., 1998). In fact, during the final stages of follicular growth, the oocyte may be susceptible to damage by ROS.

 

http://www.ncbi.nlm.nih.gov/pubmed/20663262

 

2. The DNA of the germ cells also receive lesions and ages, but in meiosis I and meiosis II and become zygote and eventually baby have an important step that fixes these lesions with a perfect repair, not the usual partial repair we have in our cells, it could also be that the genes are shuffled around in meiosis I and meiosis II that fixes the damage.

 

Why do I come to this conclusion? Because the baby is not of age 29 years old when it's born or the baby ages faster with a damaged DNA, the baby's DNA has to be perfect with no damages when it's born.

 

I don't know about meiotic repair, you would have to cite something to prove your point. Nevertheless, repair mechanisms occur to re-age chromatin in germ cells:

 

 

 

Telomeres protect and cap linear chromosome ends, yet these genomic buffers erode over an organism’s lifespan. Short telomeres have been associated with many age-related conditions in humans, and genetic mutations resulting in short telomeres in humans manifest as syndromes of precocious aging. In women, telomere length limits a fertilized egg’s capacity to develop into a healthy embryo. Thus, telomere length must be reset with each subsequent generation. Although telomerase is purportedly responsible for restoring telomere DNA, recent studies have elucidated the role of alternative telomeres lengthening mechanisms in the reprogramming of early embryos and stem cells, which we review here.

 

http://www.hindawi.com/journals/bmri/2014/925121/

 

 

Now for the conclusions for speculations 1 and 2:

 

1. For speculation 1, if we can obtain an undamaged DNA from the germ cells then we know which part of the DNA is damaged in other cells of the body and attempt to replace them with the undamaged one assuming all the DNA in our body are the same but only differs with gene expression.

2. For speculation 2, we need to identify the step that does a perfect repair to the DNA and duplicate that process for all the cells in our body.

Keep in mind that in order to change the DNA in our body we need a nanomachine, crispr also works but we need 100% accuracy. I haven't found a DNA nanomachine capable of altering DNA.

 

I thought that different humans would receive different damage depending on exposure to different ROS, different chemicals (mutagenesis), different diet, different ages (older people accumulating more hypothesised damage, different genders, different professions etc... I think you would struggle to ask 100 women to donate their ova and for your research to be performed unless the legislative authorities allow experiments on human eggs. There is a serious ethical issue here, in my opinion, which religious groups would jump upon. As for nanomachines, I don't imagine that nanoscience has yet reached this stage.

 

P.S. I feel that the DNA damage theory is a bit outdated, everyone follow a set age normally of 100+- years of age. You don't live longer or shorter because of damages done to your DNA

 

For a short chart:

1. parent undamaged DNA + parent undamaged DNA -> baby undamaged DNA

2. perfect repair(parent damaged DNA) + perfect repair(parent damaged DNA) -> baby undamaged DNA

 

How many sperm would be repaired given that there are 300 million approx. released per ejaculation?

 

The idea is good and you posted in the correct place. But, it needs a bit more background research about what is possible and what is not yet in the vista of scientific capability.

 

Well my idea is that every baby is born with a fresh copy of the DNA, there can't be any damages on it with or without repair, and mutations are out of the question for normal cases, so it is a perfect blue print. But either way, fixing the DNA would require the help of a nanomachine and as you've mentioned, they haven't reached the stage where they can freely modify DNA. To make this even more complex, the scientists aren't sure if the cells in the entire body all have the same DNA. It would be easy if the cells in the entire body all have the same DNA as an established idea, but scientists have found different. So until we find how gene is distributed across each cell there is no way of repairing. My idea is to monitor the DNA of a growing zygote at real time with laser scanning, but I'm not sure if our laser scanning technology is there yet

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The actual cells are different IIRC. I will return with a citation if I find it. IIRC, maternal cells enter the embryo during pregnancy and embryonic cells enter the mother and, in certain cases in animals, had a protective effect. Awesome and beautiful. However, and this also needs citations, some forms of electromagnetic radiation damage DNA in germ cells. Keep the ideas coming and keep posting them in Speculations.

 

 

Fetal cells migrate into the mother during pregnancy. Fetomaternal transfer probably occurs in all pregnancies and in humans the fetal cells can persist for decades. Microchimeric fetal cells are found in various maternal tissues and organs including blood, bone marrow, skin and liver. In mice, fetal cells have also been found in the brain. The fetal cells also appear to target sites of injury. Fetomaternal microchimerism may have important implications for the immune status of women, influencing autoimmunity and tolerance to transplants. Further understanding of the ability of fetal cells to cross both the placental and blood-brain barriers, to migrate into diverse tissues, and to differentiate into multiple cell types may also advance strategies for intravenous transplantation of stem cells for cytotherapeutic repair. Here we discuss hypotheses for how fetal cells cross the placental and blood-brain barriers and the persistence and distribution of fetal cells in the mother.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2633676/

 

I cannot verify the scientific accuracy of the following. I can only present it:

 

 

 

Wi-Fi Laptops Harm Sperm Motility And Increase Sperm DNA Fragmentation
Written by Christian Nordqvist

 

 

 

Males who place a laptop on their laps with the WI-FI on might have a greater risk of reduced sperm motility and more sperm DNA fragmentation, which could, in theory, undermine their chances of becoming fathers, researchers from Nascentis Medicina Reproductiva, Argentina, and the Eastern Virginia Medical School, USA, reported in the journal Fertility and Sterility this week. Sperm motility refers to the percentage of sperm in a semen sample that are moving - normally, a high percentage of all sperm should be moving (thrashing their tails and swimming).

This study was done in an artificial setting. The male participants were not tested with the laptops on their laps - semen samples were taken, placed under laptops for four hours, and then analyzed.

Previous studies had already shown that placing a laptop on a man's lap could potentially affect his fertility, especially if this occurs frequently and for long periods. The laptop can cause scrotal hyperthermia (elevated testicle temperature), which can considerably affect the quality of his sperm (Link to 2010 study).

In this new study, the authors explain that not only might the laptop-on-lap undermine semen quality, but also the Wi-Fi, if the laptop is near semen. They found that there was less damage when there was no Wi-Fi signal than when there was.

The double-whammy of the Wi-Fi signal and laptop temperature can cause:

A decrease in human sperm motility

Sperm DNA fragmentation - irreversible changes in the genetic code

Perhaps the electromagnetic radiation emitted by Wi-Fi damages the semen, the scientists suggested.

 

http://www.medicalnewstoday.com/articles/207009.php

 

Right, I really have to sleep now.

Edited by jimmydasaint
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The actual cells are different IIRC. I will return with a citation if I find it. IIRC, maternal cells enter the embryo during pregnancy and embryonic cells enter the mother and, in certain cases in animals, had a protective effect. Awesome and beautiful. However, and this also needs citations, some forms of electromagnetic radiation damage DNA in germ cells. Keep the ideas coming and keep posting them in Speculations.

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2633676/

 

I cannot verify the scientific accuracy of the following. I can only present it:

 

 

Right, I really have to sleep now.

 

Hmm, what I really want to look into is the scale of the laser scanning technology and how DNA can be visualized. I saw a clip about attosecond laser and it is pretty impressive. Keep in mind that DNA damage and DNA mutations are two different things, being near an electromagnetic radiation source does not make you age faster, speculation

 

P.S. Good night

Edited by fredreload
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