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genetics concepts > lecture 10 > Flashcards

lecture 10 Flashcards

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1
Q

what is oxidation

A

gain in oxygen, loss of hydrogen, loss of electrons

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2
Q

what is reduction

A

loss of oxygen, gain of hydrogen, gain of electrons

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3
Q

what is an oxidant

A

oxidizes another chemical by taking electrons, hydrogen, or by adding oxygen

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4
Q

what is a reductant

A

reduces another chemical by supplying electrons, hydrogen, or by removing oxygen

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5
Q

what are free radicals

A

free radicals attack and snatch energy from other cells to satisfy themselves

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6
Q

what are the most important pro-oxidants

A

ROS and RNS

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7
Q

what are some examples of free radicals

A

they have one or more unpaired electrons, so carbon center, nitrogen centered, oxygen centered, and sulfur centered

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8
Q

how are non radicals characterized?

A

has strong oxidizing potential or help to form strong oxidants

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9
Q

how long can some pro oxidants live for?

A
  • hydrogen peroxide can live for minutes
  • nitric oxide can live for seconds
  • singlet oxygen can live for microseconds
  • hydroxyl radical can live for nanoseconds
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10
Q

what are some endogenous sources of ROS

A
  • endoplasmic reticulum
  • cytoplasm
  • mitochondria
  • lysosomes
  • peroxisomes
  • plasma membrane
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11
Q

what does 90% of ROS from a cell come from?

A

the mitochondria, ETC contains several redox centers that may leak e- to oxygen

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12
Q

what is the result of oxidative damage to lipids from mitochondrial oxidative stress?

A

membrane peroxidation and decreased membrane fluidity

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13
Q

what is the result of oxidative damage to DNA from mitochondrial oxidative stress?

A

mutations and deletions

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14
Q

what is the result of oxidative damage to proteins as result of mitochondrial oxidative stress

A

oxidation of sulfhydryl groups, reactions with aldehydes and protein aggregation

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15
Q

where is NADPH oxidase mainly present in?

A

mainly in neutrophils but still present in many other cell types

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16
Q

why does NADPH oxidase make ROS on purpose?

A

because absence of ROS will result in chronic granulomatous disease

17
Q

how does lysosomes generate ROS and RNS

A

through myeloperoxidase

18
Q

how does peroxysomes generate ROS and RNS

A

through enzymes

19
Q

what does lipid peroxidation lead to?

A
  • structural changes in membranes
  • adducts/crosslinkes with non lipids
  • direct toxicity of lipid peroxidation products
  • dna damage and mutagenesis
20
Q

what are the structural changes in membranes that come from lipid peroxidation

A
  • alter fluidity and channels
  • alter membrane bound signaling proteins
  • increases ion permeability
  • disruptions in membrane dependent signaling
21
Q

what are the consequences of protein oxidation?

A
  • oxidation of catalytic sites on enzymes
  • formation of mixed sulfide bonds
  • increased susceptibility to proteolysis
22
Q

what are the consequences of DNA oxidation?

A
  • dna adducts/AP sites/strand breaks results in mutations or initiations of cancer
  • overstimulation of dna repair
23
Q

what does oxidation of catalytic sites on enzymes result in?

A

causes loss of function/abnormal function

24
Q

what exactly happens in overstimulation of dna repair?

A
  • can deplete energy reserves of cell (PARP)
  • induction of error prone polymerases
  • activation of checkpoint related signaling pathways
25
Q

what are the exogenous sources of free radicals?

A
  • irradiation
  • chemicals that react to form peroxides
  • chemicals that promote superoxide formation
  • chemicals that are metabolized to radicals
  • iron
26
Q

what are the ways oxidants can act to modify signal transduction?

A
  • heme oxidation
  • oxidation of iron sulfer centers
  • changes in thiol/disulfide redox state
  • change in conformation
  • oxidative modification of proteins
  • oxidative modification of dna
  • oxidative modification of lipids
27
Q

what does high does of oxidative stress and cell damage do?

A

-directly damages and kills cells

28
Q

what does low doses/chronic overproduction of oxidants do?

A
  • activation of cellular pathways
  • stimulation of cell proliferation
  • damage to cellular proteins, DNA and lipids
29
Q

what are defensive mechanisms against pro-oxidants?

A
  1. prevention of prooxidant formation
  2. interception of proxoxidants
  3. breaking the chain of radical reactions
  4. repair of damage caused by prooxidants
30
Q

what is the free radical theory of aging?

A

steady state accumulation of oxidative damage that increases during aging, progressive loss in efficiency of cellular processes

31
Q

what are the lessons learned from MnSod knockdown mice?

A
  • mitochondrial antioxidant enzyme peroxide is less dangerous than superoxide
  • homozygous mutant is lethal
  • 50% decrease in MnSod activity in all tissues studied
  • no compensation by other major antioxidant enzymes
32
Q

what organelle’s function is lost in SOD2 (+/-) mice

A

mitochondria:
- leads to oxidative damage to specific mito proteins
- altered mitochondrial function leads to decreased activities of ETC

33
Q

MnSOD hetero knockout mice have same lifespan but have more what?

A

cancers

34
Q

what happens when catalase levels decline with age?

A

hydrogen peroxide cannot be broken down, allows hair to be bleached from the inside out

35
Q

what is the overall importance of mitochondrial function in aging prevention?

A
  • 3-5 fold increase in point mutations and deletion in mtDNA
  • normal appearance until about 6 months, weight loss, kyphosis, decreased fat, osteoporosis
  • decreased ETC C activity and ATP production
36
Q

what kind of dna is more sensitive to oxidative damage than nuclear dna?

A

mtdna

37
Q

what chronic diseases are linked to ROS action

A
  • inflammation
  • atherosclerosis
  • ischemia/reperfusion injury
  • injury
38
Q

tissues that turn over more slowly (skeletal and heart muscle) have more what than more rapidly dividing tissues (liver)?

A

more mtdna deletion

39
Q

deletions increase with age in what two organs?

A

heart muscle and brain

genetics concepts (13 decks)

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