Cell organelles

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Cell organelles

  1. 1. Seminar onCELL ORGANELLESDr.Simi MDept of PhysiologySree Gokulam Medical College & Research Foundation.26th August 2011.
  2. 2. Introduction Discrete organelles that subserve distinct functions. Bounded by limiting membrane “Membrane-enclosed organelles” Contain enzymes.
  3. 3. History  Homogenised by disrupting cell membrane with Tween 20  Albert Claude (Nobel Prize 1974)  Marker enzymes.
  4. 4. CELL ORGANELLES  Nucleus  Endoplasmic reticulum  Golgi Apparatus  Mitochondria  Lysosomes  Peroxisome  Ribosome  Centrosomes
  5. 5. CELL ORGANELLES
  6. 6. THE NUCLEUS – stores,replicates &reads Cell’s Genetic Information. Described by Robert Brown (1831) First Discovered & Largest organelle 2-20 µm in diameter
  7. 7. Structure of Nucleus  Sorrounded by double membrane - outer membrane - inner membrane  Space b/w 2 membranes "Perinuclear Cistern"
  8. 8. Structure of Nucleus
  9. 9. Structure of Nucleus
  10. 10. Structure of Nucleus
  11. 11. THE NUCLEUSNuclear Pores “Nuclear Localisation Sequence”Nuclear Pore Complex Outer diameter : ~100 nm Resting State : ~9 nm
  12. 12. Nucleus : Storehouse of DNA  Chromosomal DNA present inside nucleus  Chromatin - Heterochromatin - Euchromatin  Transport pathways -Importins -Exportins
  13. 13. Nucleolus  described by Gabriel Valentin 1836  prominent in cells actively synthesizing proteins  Function : - RNA Processing - Ribosome synthesis
  14. 14. ENDOPLASMIC RETICULUM  Web of Tubules or Saccules sorrounding the nucleus.  “ Railway Track Appearance ” - EM George Palade (Nobel Prize 1974)  2 forms : RER & SER
  15. 15. RER SERGranular  AgranularRibosome studded Not Ribosome studdedPROTEIN SYN LIPID &STERIOD SYN Egs:Egs: Leydig cells Nissl Granules Cells of Adrenal Russel bodies Cortex Acinar cells
  16. 16. Structure of Endoplasmic Reticulum
  17. 17. ENDOPLASMIC RETICULUM  Functions: 1.Synthesis of proteins,Glycoprotein & Lipoproteins 2.Detoxification of various drugs 3.Major Reservoir of Ca2+ ions Modified ER (Sarcoplasmic Reticulum)
  18. 18. Microsomes :Formed by automatic reassembly of disrupted complex ER on cell fractionation.Func:1.Valuable tool for understanding metabolism of compounds.2.Study drug – drug interactions
  19. 19. MITOCHONDRIA - Site ofOxidative Energy Production.  “Power House of the Cell”  Richard Altman (1886)  Carl Benda coined the term  0.5 – 1 µm in diameter &  7 µm in length.
  20. 20. Structure of Mitochondria Described as a “Balloon with in a balloon” Cigar shaped organelles/ Sausage shaped organelles 2 membrane - outer membrane - inner membrane (Cristae) Lollipop shaped globular structures
  21. 21.  Define 2 distinct internal compartments - inter membrane space - matrix space Capable of “Self replication” Short Life span
  22. 22. Structure of Mitochondria
  23. 23. Mitochondrial Enzymes A. Membrane enzymes 1.Enzymes of outer membrane a) Cytochrome b5 & b5 reductase b) Fatty acid coA synthase c) Phospholipase A d) Nucleoside diphosphokinase
  24. 24. Mitochondrial Enzymes 2. Enzymes of inner membrane a) Cytochrome b,C1,C,a& a3 b) NADPH dehydrogenase c) Succinate dehydrogenase d) Electron transferring flavoproteins e) β-OH-butyrate dehydrogenase f) Carnitine – palmitoyl transferase g)All translocases
  25. 25. Mitochondrial Enzymes B. Enzymes of inter membrane space a) Adenylate kinase b) Nucleoside diphoshokinase c)Sulfite oxidase
  26. 26. Mitochondrial Enzymes C. Enzymes in the matrix a) Pyruvate dehydrogenase complex b) Citrate synthase c) Isocitrate dehydrogenase d)Malate dehydrogenase e) Fatty acid oxidation system f) Ornithine transcarbamoylase g) α-oxoglutarate dehydrogenase h) Aconitase
  27. 27. MITOCHONDRIA  Functions:  Critical manufacturer of ATP.  Programmed Cell death (Apoptosis) intracellular Ca 2+ stores.
  28. 28.  ETC (innermemb ) TCA Cycle (matrix ) β-Oxidation of FA (matrix ) Ketone body production Urea,Heme,Pyramidine syn Gluconeogenesis
  29. 29. Mitochondrial diseases dt mtdnamutations Leber hereditary optic neuropathy (LHON) NARP, Leighs disease MELAS MERRF Progressive sensorineural deafness Chronic progressive external ophthalmoplegia (PEO) Pearson syndrome Kearn-Sayre syndrome (KSS)
  30. 30. GOLGI APPARATUS – stack ofpancakes/stack of dinner plates Also called “Dyctyosome” Collection of membrane enclosed sac(abt 6 sacs ) Camillo Golgi (Nobel Prize 1906) Continuous with ER >200 enzymes Processing station
  31. 31. Structure of Golgi Apparatus
  32. 32.  Polarised structure with cis & trans sides Membrane vesicle containing proteins bud off from ER ↓ fuse with the cistern on the cis side of the apparatus. ↓ passed via other vesicles to the middle cisterns ↓finally to the cistern on the trans side, from which vesicles branch off into the
  33. 33. Functions : Site for Packaging of proteins synthesized in ER into vesicles Formation of Lysosomal enzymes Transport to other organelles Glycosylation of proteins
  34. 34. LYSOSOMES – Cell’s Trash Incinerato Discovered by Rene de Duve (Nobel Prize 1974) Large irregular structures bounded by membrane Lysosomes act as “cellular stomachs,” breaking down bacteria and the debris from dead cells that have been engulfed by a cell.
  35. 35. LYSOSOMES Proton Pump or H+-ATP ase acidic interior (ph 5.0) 40 types of enz “Acid Hydrolases” Specially adapted lys.membrane Clinical app: Gout(loss of memb integrity) Endocytic Vesicle Autophagy : “Multivesicular body”
  36. 36. LYSOSOMES Particularly abundant in cells involved in phagocytic activity. (Eg: Neutrophils & Macrophages) 3 Forms of lysosomes Primary Secondary Residual Bodies
  37. 37. Important Lysosomal EnzymesProteolytic 1.Cathepsins 2.Collagenas 3.ElastasesEnzymes esLipolytic 1.Lipases 2.Phospholip 3.Fatty acylEnzymes ase EsterasesCarbohydrat 1.α- 2. β- 3.Hyaluronid 4.Aryle splitting glycosidase galactosidas ase Sulphataseenzymes eNucleic acid 1.Ribonuclea 2.DeoxyHydrolysing e Ribonucleasenzymes eOther 1.Acid 2.Catalaseenzymes Phosphatse
  38. 38. Lysosomal storage diseases - Congenital absence of Lysosomalenzymes
  39. 39. Disease Enzyme Unique Features deficiencyFabry disease α-galactosidase A Cutaneous Angiokeratomas& hypohydrosisGaucher disease Acid β glucosidase HSM & Skeletal DysplasiaNiemann - Pick Sphingomyelinase MR,Seizures & Lung FailurediseaseTay- Sachs disease β-hexaminidase A MR,Macrocephaly & Hypercuisis in infantsHurler disease α-L-iduronidase MR,Coarse facies,CVS invPompe disease Acid α-glucosidase Myocardiopathy
  40. 40. Functions of Lysosomes:  1.Contain enzymes essential for intracellular digestion 2.Kill & remove foreign bodies 3.Acrosome :- specialised lysosome 4.Autolysis 5.remove IC pdts of metabolism
  41. 41. Ribosomes – Sites of ProteinSynthesis.  Granular structures present on surface of ER & also as free  1st observed by George Palade (1953)  Non membrane bound organelle  Measure ~ 22 x 32 nm.  Contain 85% RNA of cell
  42. 42. Ribosomes Each is made up of a large and a small subunit on the basis of their rates of sedimentation in the ultracentrifuge, the 60S and 40S subunits Polyribosomes(3-5) Func Main Site of Protein Synthesis
  43. 43. PEROXISOMES also known as microbodies “Subcellular respiratory organelles” 0.5 µm in diameter Predominantly present in Hepatocytes & Tubular Epithelial cells. surrounded by a membrane.
  44. 44.  This membrane contains a no of peroxisome-specific proteins PEROXINS- the protein Chaperones,various proteins with specifc signal sequence are directed to peroxisome.
  45. 45. Function:  Essentially contain two types of Enzymes :  Oxidases : which are active in oxidation of lipid  Catalase : which act on Hydrogen Peroxide to liberate Oxygen.
  46. 46.  Several years ago, a number of synthetic compounds were found to cause proliferation of peroxisomes by acting on receptors in the nuclei of cells. These receptors Peroxisome Proliferation Activated Receptors (PPARs)
  47. 47. Peroxisome Proliferation Activated Receptors (PPARs)• Three PPAR receptors α ,β and γ have been characterized.• When activated, they bind to DNA, producing changes in the production of mRNAs.• Mutations of the peroxisome proliferators activator receptor γ (PPARγ) cause insulin resistance
  48. 48. Lysosomes PeroxisomesLarger  SmallerFormed from Golgi Formed by self-Apparatus replication or budding from smooth ERDigestive organ of cell Detoxifying organ of the cellContain Hydrolases Contain oxidases and form H2O2Helps in intracellular Along withdigestion of food, catalase,helps in thebacteria,damaged cell detoxification of injuriousstructures etc substances
  49. 49. Applied Physiology  Perioxisomes protect from oxidative stress (OS)  1. Zellweger Syndrome - peroxisome abnormal or absent  2. Infantile Refsums Disease - few proteins are affected  3.Brown Schilders Disease -insufficient oxidn of VLCFA by perox
  50. 50. Centrosomes – Situated near the nucleus made up of 2 centrioles surrounding amorphous pericentriolar material. centrioles are short cylinders, arranged at right angles to each other.
  51. 51. Centrosomes – Microtubules in groups of 3 ,run longitudinally in the walls of each centriole. 9 of these triplets are spaced at regular intervals around the circumference.
  52. 52. Centrosomes – “microtubule-organizing centers” (MTOCs) that contain γ- tubulin. Func: monitor steps in cell division. regulate chromosome movement
  53. 53. References 1.Walter.F.Boron & Emile .L.Boulpaep Medical Physiology 2nd edition 2.Ganong’s Review of Physiology 23 rd edition 3.GK Pal Textbook of Medical Physiology 2nd edition 4.Guyton & Hall Text book of Physiology 12th edition 5.Vanders Human Physiology 8 th edition
  54. 54. References 6.Sreekumari & Vasudevan Textbook of Biochemistry 6th edition 7.Harrison’s Principles of Internal Medicine 17th edition 8.Indu Khurana Textbook of Medical physiology 9.N Geetha Textbook of Medical Physiology 2nd edition. 10.A.K Jain Textbook of Physiology 4th edition.
  55. 55. RECENT ADVANCES Organellar dysfunction in the pathogenesis of pancreatitis. Acute pancreatitis is an inflammatory disease of exocrine pancreas that carries considerable morbidity and mortality; its pathophysiology remains poorly understood. Recent findings obtained on experimental models, which reveal disordering of key cellular organelles, namely, mitochondria, autophagosomes, and lysosomes, in pancreatitis. Ref
  56. 56. RECENT ADVANCES (PPAR) represented by 3 types: PPAR alpha, PPAR beta, PPAR gamma. PPAR alpha is a key regulator of fatty acid beta- oxidation, participates in development of inflammatory reaction and atherosclerosis formation. PPAR gamma plays important role in lipid metabolism, processes of cell differentiation and growth, participates in glucose utilization and mechanisms of insulin resistance. Specific activators of PPAR gamma are glytazones Ref :http://www.ncbi.nlm.nih.gov/pubmed/14671562
  57. 57. RECENT ADVANCES The nuclear (PPAR gamma) in DM,HTN,atherosclerosis is a transcription factor that is activated by polyunsaturated fatty acids and their metabolites and is essential for fat cell formation. PPAR gamma activators such as the glitazone drugs lower glucose and lipid levels in patients with type 2 diabetes and also have antiatherosclerotic and antihypertensive effects. Ref :http://www.ncbi.nlm.nih.gov/pubmed/11395411.
  58. 58. Thank You !!!

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