mitokondria fixs

8/10/2019 Mitokondria Fixs

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Bella Rhea Lavifa. S.

(120210153038)

Sakalus Wepe

(120210153038)

Nur Kholifatun Nisa

(120210153038)

Maya Umi Hajar

(120210153050)

Saltsa Ridlotul J.

(120210153055)


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MITOCHONDI

STRUCTURE


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Mitochondria are the sites of cellular respiration, themetabolic process that generates ATP by extracting energyfrom sugars, fats, and other fuels with the help of oxygen.

Function

convert energy to forms that cells canusefor work.


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General Characteristics

Enclosed by membranes, they are not part of the endomembrane system.Mitochondria have two membranes separating their innermost spacecytosol.

The membrane proteins of mitochondria are made not by ribosomes boER, but by free ribosomes in the cytosol and by ribosomes contained worganelles themselves.

Contain a small amount of DNA that programs the synthesis of the proon the organelle's ribosomes.


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General Characteristics

Mitochondria are semiautonomous organelles that grow and reproduce cell.

Mitochondria are found in nearly all eukaryotic cells, including those animals, fungi, and most protists.

Mitochondria are about 1-10 11m long.

mitochondria moving around, changing their shapes, and fusing or dividing


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OUTER MEMBR NE

Consist of :Protein that called porin

lipid

The outer membrane is smooth, outer membrane completely permeable to

molecules, ions, and molecules of ATP ADP. In addition, the outer membrcontains enzymes involved in the biosynthesis of lipids and enzymes involtransport processes into the matrix to undergo -oxidation.


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INNER MEMBR NE

Inner Membranes is more complex in structure than the outer membbecause it contains a complex of the electron transport chain and ATsynthetase complex.Inner membrane protein involved in oxidative phosphorylation reactsynthase functioning form ATP in the mitochondrial matrix, as well a

transport proteins that regulate the passage of metabolites from the macross the membrane.


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INTERMEMBR NE SP CE

In the mitochondrial matrix contained genetic material, known as mDNA (mtDNA), ribosomes, ATP, ADP, and inorganic phosphate ionsmagnesium, calcium and potassium.


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M TRIX

The matrix is a complex mixture of enzymes that are essentiasynthesis of ATP, special mitochondrial ribosomes, RNA and

mitochondrial DNA. In addition, it has oxygen, carbon dioxidother recyclable intermediates.


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DNA MITOCHONDRIAThe mitochondria DNA en

organelle proteins that are on ribosomes within the orgorganelle-produced mRNA their amino acid sequence.

The processes of orgatranscription, protein synthereplication take place where

is located in the matrix of mit

DNA mitochondria have regulate the intracellular process, fission and mitochondria.


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Different Between DNA Mitochonand DNA Nucleus

DNA Mitochondria DNA Nucleus

Have a lot of amount than DNA nucleus Have a little of amount than DNA mi

DNA mitochondria just generated by Moms Cells DNA nucleus generated by Parents

Smaller genome Bigger genome

In mitochondria matrix In nucleus of cells

Circular DNA mitochondria, double helix. Not circular, double helix


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Metabolism Process in Mitochon

KREB CYC

TRANSPO

ELECTRON PR


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Kreb Cycle in Mitoc

kreb cycle in occurs in matrixs omitochondria.

In kreb cycle

Piruvat acid 2 ATP + 3 N

NADH

+ CO2

NADH+ CO2

NADH

FADH

CO2


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The process of kreaction :

1. condensation

2 and 3. Isomer

4. primary oxyd

5. secondary oxy

6. phosphorilati

7. third oxydatio

8 and 9. oxaloasformation


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Transport elektron


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Sistem Transpor Elektron melibatkan 5 kompprotein

Complex I (NADH-coenzyme Q oxidoreductase or NADH dehydrogenase)

Complex II (Succinate-Q oxidoreductase or Succinate dehydrogenase)

Complex III (Q-cytochrome c oxidoreductase)

Complex IV (Cytochrome c oxidase)

ATP Synthase


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10 NADH + 50 > 10 NAD+ + 10 H


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SYNTHASE

10 NADH + 502> 10 NAD+ + 10 H

2 FADH2

+ O2> 2 PAD + 2 H

20


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Life Cycle ofMitochondria


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Al h i Di


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Alzheimers Disease

Beta amyloid increases nitric

oxide, which activates DRP

causing fission and neuronaldamage. One way that motility

is impaired is with too much of

the molecule tau (which holds

microtubules together and ispart of Alzheimers pathology)

then there is no fusion and

mitochondria become shorter.

H i Di d


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Huntingtons Disorder

Too much Huntingtin protein

(the critical abnormal protein

in Huntingtons), stops fusion

and mitochondria become

shorter. Huntingtin activates

DRP increasing fission and

apoptosis Mutant Huntingincauses fragmentation and

disease.

ALS Amyotrophic Lateral Sclerosis o


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ALS Amyotrophic Lateral Sclerosis oGehrigs Disease

Mutation causes DRP fission and

inhibits axon transport of mitochondria.


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