Senescent phase of an organism lifespan is often recognized by
a) Slow metabolism
b) Cessation of reproduction
c) Decreased immunity `
d) All of those
Answer
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Hint: Cellular senescence is assumed to contribute to age related tissue and organ dysfunction and various chronic age- related diseases through various mechanisms. during a cell-autonomous manner, senescence acts to deplete the varied pools of cycling cells in an organism, including stem and progenitor cells.
Complete answer:
The end of the regenerative stage is named the Senescent Stage or Maturity. After this stage, the individual dies.
- It is marked by a general decline in metabolic activities, amid a decline in ATP synthesis and chloroplast activities.
- Decrease in DNA and RNA
- Semi permeability of cytoplasmic membranes within the cells starts declining.
- Impairment of the method of formation of the latest cells to exchange the old and dead cells.
- Due to anomalies in protein synthesis caused by senescence chromosomal aberrations and gene mutations may occur within the body cells which can be fatal.
Current physiological understanding of the senescence condition, and its positive roles in plant growth, differentiation, adaptation, survival, and reproduction, supports a definition that acknowledges senescence to be a phase of development that: (1) may be a transdifferentiation episode following the completion of growth; (2) may or might not be succeeded by death; and (3) is completely hooked into cell viability and therefore the expression of specific genes.
Additional information:
- The amount of cross- linking in the collagen molecules , leads to crystallinity and rigidity, that are observed during a general body stiffness.
- There's also a decrease within the relative amount of a mucopolysaccharide (i.e., the mixture of a protein and a carbohydrate) ground substance; a measure of this, the hexosamine–collagen ratio, has been investigated as an index of individual differences within the rate of aging as the age increases.
- A crucial consequence of those changes is decreased permeability of the tissues to dissolved nutrients, hormones, and antibody molecules.
- At the further extreme of senescence are even slower aging patterns that I even have provisionally called negligible senescence. In these species, there's no evidence of physiological dysfunctions at advanced ages, no acceleration of mortality during adult life, and no recognized characteristic limit to lifetime.
- A promising example of negligible senescence from the vertebrates is that of the rockfish genus Sebastes, a scorpaenidae with several species that achieve ages greater than 100 years. The age is estimated from measurements of otolith rings in conjunction with natural radioisotopes
So the correct answer is 'All of those'.
Note: The findings derived from an examination of ARCs in physiological systems of the body also produce a blurring between senescence and disease. Clinical and pathologic changes within the brains of individuals with sporadic Alzheimer's disease (e.g., brain weight and volume declines, glutamatergic hyperactivity, neocortical neuron loss, accumulation of senile plaques and neurofibrillary tangles) also are found within the brains of "normal aged" people
Complete answer:
The end of the regenerative stage is named the Senescent Stage or Maturity. After this stage, the individual dies.
- It is marked by a general decline in metabolic activities, amid a decline in ATP synthesis and chloroplast activities.
- Decrease in DNA and RNA
- Semi permeability of cytoplasmic membranes within the cells starts declining.
- Impairment of the method of formation of the latest cells to exchange the old and dead cells.
- Due to anomalies in protein synthesis caused by senescence chromosomal aberrations and gene mutations may occur within the body cells which can be fatal.
Current physiological understanding of the senescence condition, and its positive roles in plant growth, differentiation, adaptation, survival, and reproduction, supports a definition that acknowledges senescence to be a phase of development that: (1) may be a transdifferentiation episode following the completion of growth; (2) may or might not be succeeded by death; and (3) is completely hooked into cell viability and therefore the expression of specific genes.
Additional information:
- The amount of cross- linking in the collagen molecules , leads to crystallinity and rigidity, that are observed during a general body stiffness.
- There's also a decrease within the relative amount of a mucopolysaccharide (i.e., the mixture of a protein and a carbohydrate) ground substance; a measure of this, the hexosamine–collagen ratio, has been investigated as an index of individual differences within the rate of aging as the age increases.
- A crucial consequence of those changes is decreased permeability of the tissues to dissolved nutrients, hormones, and antibody molecules.
- At the further extreme of senescence are even slower aging patterns that I even have provisionally called negligible senescence. In these species, there's no evidence of physiological dysfunctions at advanced ages, no acceleration of mortality during adult life, and no recognized characteristic limit to lifetime.
- A promising example of negligible senescence from the vertebrates is that of the rockfish genus Sebastes, a scorpaenidae with several species that achieve ages greater than 100 years. The age is estimated from measurements of otolith rings in conjunction with natural radioisotopes
So the correct answer is 'All of those'.
Note: The findings derived from an examination of ARCs in physiological systems of the body also produce a blurring between senescence and disease. Clinical and pathologic changes within the brains of individuals with sporadic Alzheimer's disease (e.g., brain weight and volume declines, glutamatergic hyperactivity, neocortical neuron loss, accumulation of senile plaques and neurofibrillary tangles) also are found within the brains of "normal aged" people
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