The elixir of life
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Genes that affect replicative life span in yeast also influence aging in other organisms. A comprehensive analysis of replicative life span was performed on 4,698 single-gene deletion yeast strains, demonstrating conservation of longevity pathways between yeast and nematodes. Specifically, deletion of the LOS1 gene, which encodes a tRNA exporter, extended yeast lifespan by 60% due to LOS1 being excluded from the nucleus under dietary restriction and mTOR inhibition.
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Pathogenesis of cell injury By Rohit Kumar Trivedi
Pathogenesis of Cell Injury
Pathophysiology Google Classroom Code: vbwvno4
Google Classrom Link: https://classroom.google.com/c/MzM1NjcyOTIxMjgy?cjc=vbwvno4
FACEBOOK: https://www.facebook.com/rohitkrtrivedi
INSTAGRAM: https://www.instagram.com/rohit_kumar_trivedi
SLIDESHARE: https://www.slideshare.net/Rohittrivedi321
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This study examined the effects of two mitochondrial metabolites, acetyl-L-carnitine and alpha-lipoic acid, on age-related hearing loss in rats. Twenty-one aged rats were divided into three groups receiving one of the metabolites or a placebo daily for 6 weeks. Hearing was tested before and after, and tissue samples were analyzed. The control group showed expected age-related hearing decline, while treated groups experienced reduced progression. Acetyl-L-carnitine significantly improved hearing thresholds. Both metabolites reduced mitochondrial DNA damage associated with aging and hearing loss. The results suggest these compounds can delay age-related declines by protecting mitochondrial function.
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Pathogenesis of cell injury By Rohit Kumar Trivedi
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FACEBOOK: https://www.facebook.com/rohitkrtrivedi
INSTAGRAM: https://www.instagram.com/rohit_kumar_trivedi
SLIDESHARE: https://www.slideshare.net/Rohittrivedi321
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2) 21 aged rats were divided into groups receiving one of the metabolites or a control, and hearing was tested before and after.
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- The objective of the study was to investigate the cytotoxic effects of 15 synthetic flavonoids against human leukemia cell lines and understand the mechanism of cell death, including caspase activation, MAPK pathway activation, and reactive oxygen species generation.
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2. Inducing oxidative stress which can damage DNA and proteins.
3. Specifically interacting with protein targets like ion channels to disrupt cellular processes.
4. Inhibiting cellular respiration by blocking enzymes involved in ATP production, leading to energy depletion and cell death.
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Biochemistry of Aging
Presented by Shanzay Annum Malik
Aging
Gradual change in an organism that leads to increased risk of weakness, disease, and death over the entire adult life span of any living thing.
There is a decline in biological functions and in ability to adapt to metabolic stress.
Changes in organs include
reduced immunity,
loss of muscle strength,
decline in memory and cognition,
loss of colour in the hair
elasticity in the skin.
Gerontology and Geriatrics
Gerontology is concerned with the changes that occur between maturity and death along with factors that influence these changes.
Geriatrics focuses on health care of elderly people and promote health by preventing and treating diseases and disabilities in older adults.
Factors of Aging
Mitochondria: main unit of chemical power supply
During the synthesis of macroergical bio-molecules(high energy releasing potentials e.g. ATP) free radicals are being produced as the by-product.
Free radicals released in large quantities cause intercellular oxidative stress (e.g. oxidative damage of mitochondria)
damaging mitochondria and cause early apoptosis
Free radical
A molecule that contains one or more unpaired electrons &is capable of independent existence.
Eg : Superoxide H2O2,
hydroperoxy radical (HOO+2 )
lipid peroxideradical (ROO)
Nitric oxide (NO)
Harmful effect of free radicals
Because of their reactive nature, free radical can provoke inflammation or altered cellular function through
Lipid peroxidation
Protein modification
DNA modification
Lipid peroxidation product:
React with amino acid mainly CYS, HIS,LYS to modify protein structure & function.
Can crosslink lipid in cell membrane interrupting structure & fluidity.
Protein modification
DNA modification :
Free radical induced DNA damage includes
strand break.
DNA protein crosslink.
large range of base & sugar modification.
Telomeres
Repetitive DNA sequences at the ends of all human chromosomes
aging cells have shorter telomeres
length differs between species
in humans 8-14kb long
Telomeres are thought to be the "clock" that regulates how many times an individual cell can divide.
Telomeric sequences shorten each time the DNA replicates.
Once the telomere shrinks to a certain level, the cell can no longer divide. Its metabolism slows down, it ages, and dies
Apoptosis and Necrosis
There are two ways that a cell can die:
Necrosis occurs when a cell is damaged by an external force, such as poison, a bodily injury, an infection or getting cut off from the blood supply (which might occur during a heart attack or stroke). When cells die from necrosis, it's a rather messy affair. The death causes inflammation that can cause further distress or injury within the body.
Apoptosis or programmed cell death
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They break down the cellular components needed for surviva
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1) The study investigated the effects of two mitochondrial metabolites, alpha-lipoic acid and acetyl-L-carnitine, on age-related hearing loss in rats.
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This document discusses how cancer cells have altered metabolism that promotes their growth and survival. Oncogenic mutations activate pathways like PI3K/Akt/mTOR that increase nutrient uptake and biosynthesis, putting cancer cells in a constant state of metabolic stress and hunger. This metabolic stress activates autophagy, which recycles cellular components and supports cancer cell metabolism and survival during starvation or chemotherapy. Autophagy degradation provides nutrients and building blocks and removes damaged mitochondria that could increase harmful reactive oxygen species. Cancer cells with oncogenic mutations like in Ras show increased basal autophagy that is essential for their survival. This suggests targeting autophagy may be an effective strategy to treat cancers dependent on it.
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Protein folding and proteostasis
A physical process by which a polypeptide chain (sequence of amino acids) folds into its characteristic & functional native structure from a random coil or a linear sequence.
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This document discusses protein misfolding and diseases associated with misfolded proteins. It begins with an introduction to protein folding and reasons why proteins may misfold. Key points include that protein folding is influenced by mutations and external factors. Diseases caused by misfolded proteins are mentioned, such as Alzheimer's and Parkinson's disease. Therapeutic approaches aim to inhibit aggregation, interfere with post-translational changes, and upregulate molecular chaperones. Issues to resolve include developing tools to predict folding effects and determining the balance between protein elimination and accumulation. The conclusion emphasizes ongoing research to understand protein misfolding mechanisms and develop novel therapies.
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This document discusses oxidative stress and various neurological conditions where free radicals may play a role, such as Alzheimer's disease, Parkinson's disease, and stroke. It then summarizes several antioxidants that have been studied for treating these conditions, including vitamin E, tirilazad, ebselen, coenzyme Q10, idebenone, and combinations of antioxidants for ALS and mitochondrial diseases. While some studies showed benefits, the evidence is limited and more research is still needed on dosing schedules. Cocktail antioxidant regimes may not be cost-effective options.
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- Caspases, which are key proteins that transduce and execute apoptotic signals. They activate initiators and executors of apoptosis.
- MAPKs, the three major pathways (ERK, JNK/SAPK, p38MAPK) that regulate cell proliferation, survival, and differentiation.
- The objective of the study was to investigate the cytotoxic effects of 15 synthetic flavonoids against human leukemia cell lines and understand the mechanism of cell death, including caspase activation, MAPK pathway activation, and reactive oxygen species generation.
Print slidess
Chemicals can cause cellular dysfunction through several mechanisms:
1. Causing DNA or protein adducts which can lead to mutations, dysfunction, and uncontrolled cell proliferation.
2. Inducing oxidative stress which can damage DNA and proteins.
3. Specifically interacting with protein targets like ion channels to disrupt cellular processes.
4. Inhibiting cellular respiration by blocking enzymes involved in ATP production, leading to energy depletion and cell death.
AUTOPHAGY LINKS TO VARIOUS DISEASES
Autophagy is a normal cellular process that maintains homeostasis through degradation and recycling of cellular components. It plays a dual role in cancer and other diseases. The document discusses three main types of autophagy and the steps of autophagosome formation. It explores the link between autophagy and diseases like cancer, diabetes, and neurodegenerative disorders. Specifically, it examines the role of autophagy in diabetic neuropathy and potential interventions that target the autophagy process.
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SEMINARIO BIOLOGÍA MOLECULAR. 3′-Hydroxy-3,4′-dimethoxyflavone-induced cell d...
Similar to The elixir of life
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A resume of the role of stem cells in tissue maintenance ,tissue damage , and the factors affecting stem cell integrity .
Biochemistry of Aging
This document summarizes the key biochemistry processes involved in aging. It discusses how aging leads to a decline in biological functions over time due to factors like mitochondrial damage and free radicals. This causes changes in organs such as reduced immunity and loss of muscle strength. The document also examines specific aging-related processes like telomere shortening, apoptosis, protein and DNA modification from free radical damage, and diseases that affect the elderly like progeria. Gerontology focuses on studying these age-related changes while geriatrics aims to promote health in older adults.
Biochemistry of aging
Biochemistry of Aging
Presented by Shanzay Annum Malik
Aging
Gradual change in an organism that leads to increased risk of weakness, disease, and death over the entire adult life span of any living thing.
There is a decline in biological functions and in ability to adapt to metabolic stress.
Changes in organs include
reduced immunity,
loss of muscle strength,
decline in memory and cognition,
loss of colour in the hair
elasticity in the skin.
Gerontology and Geriatrics
Gerontology is concerned with the changes that occur between maturity and death along with factors that influence these changes.
Geriatrics focuses on health care of elderly people and promote health by preventing and treating diseases and disabilities in older adults.
Factors of Aging
Mitochondria: main unit of chemical power supply
During the synthesis of macroergical bio-molecules(high energy releasing potentials e.g. ATP) free radicals are being produced as the by-product.
Free radicals released in large quantities cause intercellular oxidative stress (e.g. oxidative damage of mitochondria)
damaging mitochondria and cause early apoptosis
Free radical
A molecule that contains one or more unpaired electrons &is capable of independent existence.
Eg : Superoxide H2O2,
hydroperoxy radical (HOO+2 )
lipid peroxideradical (ROO)
Nitric oxide (NO)
Harmful effect of free radicals
Because of their reactive nature, free radical can provoke inflammation or altered cellular function through
Lipid peroxidation
Protein modification
DNA modification
Lipid peroxidation product:
React with amino acid mainly CYS, HIS,LYS to modify protein structure & function.
Can crosslink lipid in cell membrane interrupting structure & fluidity.
Protein modification
DNA modification :
Free radical induced DNA damage includes
strand break.
DNA protein crosslink.
large range of base & sugar modification.
Telomeres
Repetitive DNA sequences at the ends of all human chromosomes
aging cells have shorter telomeres
length differs between species
in humans 8-14kb long
Telomeres are thought to be the "clock" that regulates how many times an individual cell can divide.
Telomeric sequences shorten each time the DNA replicates.
Once the telomere shrinks to a certain level, the cell can no longer divide. Its metabolism slows down, it ages, and dies
Apoptosis and Necrosis
There are two ways that a cell can die:
Necrosis occurs when a cell is damaged by an external force, such as poison, a bodily injury, an infection or getting cut off from the blood supply (which might occur during a heart attack or stroke). When cells die from necrosis, it's a rather messy affair. The death causes inflammation that can cause further distress or injury within the body.
Apoptosis or programmed cell death
When a cell is compelled to commit suicide proteins called caspases go into action.
They break down the cellular components needed for surviva
ros [].pptx
Reactive oxygen species (ROS) are highly reactive molecules formed from oxygen that can damage cells. They are produced endogenously through cellular processes like mitochondrial electron transport or immune cell activity, and exogenously through environmental exposures. At moderate levels ROS act as signaling molecules, but excess can cause oxidative stress. Antioxidants like enzymes and vitamins neutralize ROS and prevent cellular harm. The seminar discussed sources and functions of ROS as well as the protective role of antioxidants in maintaining redox balance in the body.
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Novel drug target-Enzymes
ROCK (Rho-associated protein kinase) is a kinase enzyme that regulates the shape and movement of cells through effects on the cytoskeleton. It has two isoforms, ROCK1 and ROCK2, that are highly similar. ROCK phosphorylates several substrates that regulate actin filament organization and cellular contractility. Due to its role in many physiological processes, ROCK has implications for diseases like diabetes, neurodegeneration, pulmonary hypertension and cancer. ROCK inhibitors thus have potential as novel therapeutics.
Cellular ageing
Describes the process of ageing in cells, factors affecting cells like telomere, free radicals, oxidative stress, DNA damage, environmental factors, proteostasis, mitochondrial disfunction etc are described
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Reactive oxygen species and its role in periodontal
This document summarizes reactive oxygen species (ROS) and their role in periodontal diseases. It discusses the origin of ROS and free radicals from neutrophils and their tissue-damaging effects through lipid peroxidation, protein and DNA damage. Biomarkers of ROS-mediated tissue destruction include MDA, isoprostanes for lipid damage and 8-OHdG for DNA damage. The body's antioxidant defense system works to reduce ROS, but studies show lower antioxidant levels and higher ROS biomarkers in the serum, saliva and gingival crevicular fluid of periodontitis patients, providing evidence of ROS-mediated tissue destruction in periodontal disease.
Reactive oxygen species
This document discusses reactive oxygen species (ROS) and antioxidants in biology and medicine. It defines key terms and explores the origins and effects of different ROS like superoxide, nitric oxide, and hydroxyl radicals. It also examines the mechanisms of tissue damage caused by ROS and the roles of antioxidant defense systems in preventing damage. Biomarkers of oxidative stress and lipid, DNA, and protein damage are reviewed. Evidence suggests ROS contribute to periodontal tissue destruction in periodontitis through lipid peroxidation and oxidative damage.
cell and its organelles
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This document discusses cellular adaptation, injury, and death. It covers topics like hyperplasia, hypertrophy, atrophy, metaplasia, causes of cell injury including hypoxia and free radicals, necrosis and apoptosis. It provides detailed descriptions of the morphological changes that occur during cellular injury and the mechanisms of necrosis, apoptosis and intracellular accumulation.
cellularageing-200601173158 (1).pdf
Cellular ageing is the progressive decline in cellular function and viability caused by genetic abnormalities and the accumulation of damage over time. There are several theories that attempt to explain the aging process, including evolutionary, molecular, cellular, and systemic theories. At the cellular level, ageing is caused by DNA damage from both endogenous and exogenous sources, as well as telomere shortening after each cell division. Other factors that contribute to cellular ageing include defective protein homeostasis, disrupted nutrient sensing pathways, and the accumulation of damaged or mutated proteins and organelles within the cell over time. Premature ageing disorders provide insights into how defects in certain genes involved in DNA repair and maintenance can accelerate the normal ageing process.
Cellular ageing
Cellular ageing is the progressive decline in cellular function and viability caused by genetic abnormalities and the accumulation of damage over time. There are several theories that attempt to explain the aging process, including evolutionary, molecular, cellular, and systemic theories. At the cellular level, ageing is caused by DNA damage from both endogenous and exogenous sources, as well as telomere shortening after each cell division. Other factors that contribute to cellular ageing include defective protein homeostasis, disrupted nutrient sensing pathways, and a decline in cellular repair mechanisms. Premature ageing disorders provide insights into how disrupting certain ageing processes can accelerate ageing. While cellular senescence limits cell proliferation and acts as a tumor suppressor, it is
Basics of cellular aging and
1. Cellular aging results from a progressive decline in the proliferative capacity and lifespan of cells due to accumulation of damage from genetic and environmental factors over time.
2. Key mechanisms of cellular aging include shortening of telomeres, accumulation of aging pigments, free radicals, and changes in gene expression through epigenetic alterations.
3. Apoptosis is a tightly regulated form of programmed cell death where cells activate enzymes to degrade their own nuclear DNA and proteins, then break into fragments that are cleared by phagocytes before potential inflammation from secondary necrosis.
Age changes in oral tissues
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Anti oxidants in resp med
Oxidative stress occurs when there is an imbalance between reactive oxygen species (ROS) and antioxidants, leading to cellular damage. ROS are generated through normal metabolic processes and environmental exposures like cigarette smoke and air pollution. They play roles in signaling but can cause harm in excess. Antioxidants like superoxide dismutase and glutathione normally counteract ROS. In respiratory diseases like asthma, emphysema, and pulmonary fibrosis, oxidative stress is elevated due to increased ROS and/or depleted antioxidants, contributing to airway inflammation and tissue injury. This oxidative damage may be a therapeutic target through antioxidants or reducing environmental oxidant exposures.
GENERATION AND ROLE OF FREE RADICAL IN VARIOUS (1).pptx
This document provides an overview of free radicals, including their sources, formation, targets, and role in pathogenesis. Some key points:
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- When free radical production overwhelms the body's antioxidant defenses, oxidative stress occurs and plays a role in chronic diseases. Free radicals can damage lipids, proteins, and DNA.
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- Oxidative stress contributes to diseases like cancer, cardiovascular issues
Sperm dna fragmentation - infertility centre in jaipur
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Free radical reactions are expected to produce progressive adverse changes that accumulate with age throughout the body. Such “normal” changes with age are relatively common to all.
However, superimposed on this common pattern are patterns influenced by genetics and environmental differences that modulate free radical damage.
These are manifested as diseases at certain ages determined by genetic and environmental factors.
Cancer and atherosclerosis, two major causes of death, are salient “free radical” diseases. Cancer initiation and promotion is associated with chromosomal defects and oncogene activation. It is possible that endogenous free radical reactions, like those initiated by ionizing radiation, may result in tumor formation.
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Event Link:- https://meetups.mulesoft.com/events/details/mulesoft-mysore-presents-mule-event-processing-models/
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● What is event processing in MuleSoft?
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● Distinction between the reactive, parallel, blocking & non-blocking processing
For Upcoming Meetups Join Mysore Meetup Group - https://meetups.mulesoft.com/mysore/YouTube:- youtube.com/@mulesoftmysore
Mysore WhatsApp group:- https://chat.whatsapp.com/EhqtHtCC75vCAX7gaO842N
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Shivani Yasaswi - https://www.linkedin.com/in/shivaniyasaswi/
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Shubham Chaurasia - https://www.linkedin.com/in/shubhamchaurasia1/
Giridhar Meka - https://www.linkedin.com/in/giridharmeka
Priya Shaw - https://www.linkedin.com/in/priya-shaw
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9
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The elixir of life
- 1. The Elixir of Life Presented by Rachel Jacob Z00-15-05-10
- 2. • RLS is the yeast homologue to age in higher eukaryotes • Replicative Life Span (RLS) is a phenotypic characteristic • RLS is the number of daughter cells produced prior to irreversible cell cycle arrest • Due to asymmetric cell division
- 3. • Accumulation of Senescence factors • Accumulation of Extra chRomosomal DNA Circles (ERCs) • Damaged nuclear pore complex • Dysfunctional Mitochondria
- 7. Reduction in nutrient availability in the absence of malnutrition. Promotes longevity and healthy aging in organisms ranging from yeasts to humans. Inhibition of mechanistic target of rapamycin (mTOR) through DR
- 9. Reactive oxygen species (ROS) are a family of compounds that can Oxidatively damage cellular macromolecules which influence lifespan. Reactive Oxygen Species (ROS) generated from mitochondrial respiration are the primary drivers of aging in humans and other species.
- 10. Autophagy is a cellular recycling process that can remove aged or damaged cellular components. Autophagic activity is regulated by many factors, such as the TOR pathway, Sirtuins, and caloric restriction.
- 11. c AMP dependent pKA pathway is a nutrient response pathway to be implicated in lifespan extension from DR in yeast. c AMP pathway is stimulated by the presence of Glucose.
- 16. LOS 1
- 17. Genes that affect Replicative Life Span (RLS) in Saccharomyces cerevisiae also affect aging in other organisms such as C.elegans and Mus musculus.
- 18. “A Comprehensive Analysis of Replicative Lifespan in 4,698 Single-Gene Deletion Strains Uncovers Conserved Mechanisms of Aging” Brian Kennedy et al. in Cell Metabolism. Published on October 8 2015 doi:10.1016/j.cmet.2015.09.008
- 19. Systematic analysis of yeast RLS in a set of 4,698 viable single-gene deletion strains was performed. Full genome-to-genome comparison demonstrated a significant conservation in longevity pathways between Yeast and Caenorhabditis elegans.
- 20. • Deletion of tRNA exporter LOS1 robustly extended lifespan by 60 per cent. • Dietary restriction (DR) and inhibition of mechanistic Target of Rapamycin (mTOR) exclude Los1 from the nucleus.
- 22. Thank You!
Editor's Notes
- Autophagy is important for the control of the quality of proteins and organelles for maintaining cell function. Damaged proteins and organelles accumulate in aged organs. The inhibition of autophagy decreases the lifespan, and on the other hand, the induction of autophagy can prolong the lifespan. Pharmacological intervention to extend the lifespan has demonstrated a crucial role for autophagy. The level of autophagic activity decreases with aging.
- The loss of sensitivity of AMPK activation to cellular stress impairs metabolic regulation, increases oxidative stress and reduces autophagic clearance. These age-related changes activate innate immunity defence, triggering a low-grade inflammation and metabolic disorders.