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Life signals from Napoleon era

Author: Danut Dragoi, PhD

Introduction

On a movie documentary about St Helena island, see link in here we learn about the natural habitat of that island since Napoleon landed there in 1815 when the British government selected Saint Helena as the place of exile, see link in here. On same island while Napoleon was in exile on same island, I am pretty sure he met Jonathan, now a 201-year-old giant tortoise. The age may not be very accurate but as at December 2015 Jonathan was reported to be “alive and well”. “He’s blind from cataracts, has lost his sense of smell, and so cannot detect food (his fellow giants mug me and can detect the tiniest morsel dropped on the ground), but he has retained excellent hearing.”, see link in here  . It is reported that there are tortoises that lived longer than 250 years, see link in here . These creatures that live so long may have an explanation, see link in here.

The picture below shows Jonathan and a visitor in very recent days, see link in here .

Snt Helena Turtle

Image SOURCE: https://youtu.be/yXG5OyziGzo

It is interesting how looked Jonathan tortoise in 1900, see link in here

Some people explain the longevity of Jonathan in different ways, one is his protective shell against UV and other environmental radiation, the other relates to metabolism and DNA repair.

Protective shell against UV and other environmental radiation

Since life on the Earth is threaten daily not only by UV but also by cosmic radiation with the devastating effects on life affected by various cancers, the tortoises seemed to escape this path by using their natural shielding, the shell. This is as a life signal from the past which can be interpreted as a natural protection against any environmental harmful factors. The cosmic radiation may be a key and a topic for further research on human life on Earth can be considered.

DNA Repair and Ageing, Life-span, diet and DNA

Why do tortoises live so long? It is not uncommon for a giant tortoise to reach 150 years in age. Some have even suggested there is a Galapagos tortoise old enough to have met Charles Darwin. Darwin himself only lived for half as long – still rather longer than the average human of his day. Since the 1800s, improvements in lifestyle and medicine now mean that humans in developed nations live on average 20 years longer. Not quite tortoise potential, see link in here.

Scientists have come up with some interesting ideas, which might cast light on why different species have different life-spans. One such theory relates to metabolism. Humans and other mammals have higher metabolic rates than their reptilian counterparts. We make all our own heat rather than absorbing it from the sun. As we breathe in the air around us, oxygen diffuses into our cells, fuelling the combustive process of respiration, the driving force behind our metabolism, growth and development. see link in here.

While we make energy from food in this way, hazardous by-products are created that can damage our DNA, so-called reactive-oxygen species (ROS). The higher the metabolic rate, the greater the damage potential and the more likely our cells are to mutate and malfunction. Reptiles, like tortoises might be less susceptible to DNA damage caused by ROS, because they produce lower levels of these reactive chemicals. see link in here.

We don’t know how much DNA damage speeds up ageing or indeed how much it is relevant to the natural ageing process, but recent research suggests that knowing more about our genetic maintenance might improve our quality of life. There’s no point in living as long as a tortoise if you’re not fit enough to enjoy it, see link in here.

Life-span, diet and DNA

Dietary research on mice, monkeys, rats, spiders, fruit-flies and worms further emphasizes the link between metabolism and life-span. Severely restricting calorie intake (60-70% of our daily intake) can prolong life-span, given sufficient vitamins, minerals and other nutrients. The thinking is that fewer calories will result in a lower metabolic rate, less ROS and therefore less damage to DNA. see link in here.

“That is the secret behind calorie restriction prolonging life-span in a natural manner,” says Jan Hoeijmakers (Department of Cell Biology and Genetics, Erasmus, Rotterdam), whose team is researching the role of DNA damage in ageing. He and others support the view that calorie restriction reduces metabolism, lowering ROS and the resultant stress on the DNA repair system thereby keeping cells healthier for longer.see link in here.

Reactive oxygen species are charged molecules that can disrupt or alter energy bonds between other molecules. Chemicals like superoxide and hydrogen peroxide result from respiration in the powerhouses (mitochondria) of our cells. Neither chemical alone can harm DNA, but in the presence of iron or copper ions they form hydroxyl radicals that can damage organic bases (A, T, C or G) in DNA, which can translate through to protein function. see link in here.

Removal of damaged bases is estimated to occur 20 000 times a day in each body cell. Needless to say adequate measures must be taken to prevent chaos in the cell. Luckily we have a network of sophisticated DNA repair systems policing our genes and keeping genetic order. Scientists have identified well over a hundred genes involved in the various DNA repair pathways that both signal damage and effect a repair response. Ongoing research efforts continue daily to find pieces of this complex molecular jigsaw puzzle. see link in here.

While DNA damage hasn’t been shown to cause ageing directly, a number of rare human disorders, caused by mutations in DNA repair genes, include symptoms of premature ageing. Jan Hoeijmaker’s team at Erasmus, in a recent Nature publication (Niedernhofer et al 2006), describe a new ageing syndrome in a teenage boy who encountered the fate of an old man before he even reached puberty. see link in here.

The patient had mutation in a gene (called XPF) involved together with its partner ERCC1 in DNA repair. The two-protein complex (called XPF/ERCC1) protects against the kind of DNA damage caused by UV sunlight, which can mess up the DNA sequence (see DNA in human disorders). Mutations in the XPF gene are known to cause a rare condition known as Xeroderma pigmentosum (XP). Patients with XP are so sensitive to sunlight, they must completely cover themselves when they go outside and when indoors, live with curtains and shutters drawn. Failure to do so results in skin-cancer. see link in here.

Patient ‘XFE’ was sensitive to sunlight, but more dramatic in his case, was the wizened, wasted appearance he developed by the age of 15, not characteristic of XP patients, who usually die from cancer later in life. He was blind and deaf and many of his body organs had wasted away. Jan explains that mutations in the XPF gene can be mild to extreme, mild mutations associating with cancers, in particular skin cancer, and severe mutations with premature ageing, as in the case of patient ‘XFE’. see link in here.

The Dutch team has created mouse models defective in the XPF/ERCC1 protein complex that map closely to the clinical conditions of patient ‘XFE’. Mice with a defect in the ERCC1 protein also age prematurely and die after a few weeks. When Jan’s group analysed genes in the liver of defective mice, well-over 1500 genes showed altered activity when compared to age-matched normal mice. The team confirmed that the same alterations to liver, a key player in metabolism, occur in naturally aged mice. see link in here.

Among such changes is a low level of insulin-like growth factor-1(IGF-1). This protein-hormone, made and released into the bloodstream by the liver, normally boosts growth. Jan argues that the low levels of IGF-1 in aged and DNA-repair defective mice embody a stress-response that shifts priority from growth and development to maintenance and repair in the face of increasing DNA damage. see link in here.

“Using the rapidly aging mouse mutants, our intention is to efficiently identify compounds in food or drugs that improve the heath status and life span of the mice. So I started up a company called DNage (recently acquired by Pharming ), whose mission is to provide solutions for medical/health care problems associated with ageing.” see link in here.

The links between the growth hormone axis, the DNA repair system and the ‘ageing process’ warrant further research, of which the above mentioned studies are an important step in the right direction. Jan is hopeful that with a better understanding of DNA damage, diet and ageing, we can significantly improve the quality of life for those living longer, see link in here.

Watch video

https://youtu.be/yXG5OyziGzo

It is interesting how looked Jonathan tortoise in 1900, see link in here http://www.bbc.com/news/magazine-26543021

Source

https://youtu.be/yXG5OyziGzo

Meet Jonathan, St Helena’s 182-year-old giant tortoise

.http://www.bbc.com/news/magazine-26543021

https://en.wikipedia.org/wiki/Saint_Helena

https://en.wikipedia.org/wiki/Jonathan_(tortoise)

http://www.slate.com/articles/news_and_politics/explainer/2006/03/why_do_giant_tortoises_live_so_long.html.

http://www.dna-repair.nl/start/public_info/?Introduction:DNA_Repair_and_Ageing

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