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SUBJECT: ADVANCED PHARMACOLOGY –II
GUIDED BY
Dr. DEEPARANI UROLAGIN
RR COLLEGE OF PHARMACY
RR LAYOUT, CHIKKABANAVARA,
BANGALORE 560090
PRESENTED BY
ANSARI AASHIF RAZA
(IInd semester , M.PHARM)
DEPARTMENT OF PHARMACOLOGY
FREE RADICALS PHARMACOLOGY
1 YEAR M PHARM ANSARI AASHIF RAZA
1
Free radicals:
• A free radical is defined as any chemical species that contains
unpaired electron (s) in its outer orbit.
INTRODUCTION
1 YEAR M PHARM ANSARI AASHIF RAZA
2
• Atomic or molecular species with unpaired electrons on an otherwise
open shell configuration.
• These unpaired electrons are usually highly reactive, so radicals are
likely to take part in chemical reactions.
• Through a chain of oxidative reactions to cause tissue injury, like
lipids, proteins, and nucleic acids, free radical damage is associated
with oxidative damage, causing direct cellular injury by inducing
lipid and protein peroxidation and damaging nucleic acids.
1 YEAR M PHARM ANSARI AASHIF RAZA
3
FREE RADICALS
A]Superoxide (O2 . -) B]Hydroxyl Radical (OH. )
C] Peroxyl ( R00. ) D]NO
Physiological Stimuli that Form Free Radicals
Normal respiration –
• O2 – Superoxide,
• H2O2 – Hydrogen Peroxide
• HOCL – Hypochlorous acid
• NO – Nitric Oxide
Transition metals present inside our body when are in free form behave
as free radicals. Fe2+, Cu+
1 YEAR M PHARM ANSARI AASHIF RAZA 4
 Pathological Stimuli that Form FRs
Radiation →Breaks the water inside our body: H2O =H+ + OH-
• Metabolism of drugs → CCl3
• Transition Metals → Cu+, Fe2+
• Ultraviolet rays
• Emotional stress
 Reactive Oxygen Species (ROS)
• superoxide anion (O2 - ) • hydroxyl radical (·OH)
• Hypochlorous acid ( HOCl) • Singlet Oxygen (1DgO2) - oxygen at an excited state
• Hydrogen Peroxide (H2O2).
H2O2 is considered a reactive oxygen species because of its ability to generate highly
reactive hydroxyl free radicals through interactions with reactive transition metals Fe and
Cu. 1 YEAR M PHARM ANSARI AASHIF RAZA
5
REACTIVE OXYGEN SPECIES (ROS):
 These are free radicals derived initially from oxygen. But as they do not contain
unpaired electrons in their outermost orbit, they do not qualify as free radicals and so
are referred to separately as ROS.
E.g.- H2O2, HOCL, NO. Free radicals are formed inside our body by both
PHYSIOLOGICAL (Natural) and PATHOLOGICAL stimuli.
Role of ROS
1. important role in a number of physiological processes, including the
intracellular killing of bacteria by neutrophil granulocytes detoxification by
the liver
2. prostaglandin production and certain cell signaling processes
3. During the oxidative phosphorylation or one-electron reduction of O2 in the
mitochondria (respiration) as the natural byproduct
1 YEAR M PHARM ANSARI AASHIF RAZA 6
ROLE OF FREE RADICALS IN ETIOPATHOGENESIS
o When produced in excess, free radicals and oxidants generate a
phenomenon called oxidative stress, a deleterious process that
can seriously alter the cell membranes and other structures such
as proteins, lipids, lipoproteins, and DNA.
o Oxidative stress results from an imbalance between the
formation and neutralization of ROS/RNS.
1 YEAR M PHARM ANSARI AASHIF RAZA
7
Cancer: Like radiation and carcinogens, free-radical
oxidation breaks strands of DNA. The breaks are repaired,
but some mistakes occur leading to mutations. These
genetic mutations can cause cancers. The age-related
increase in cancer rates might have something to do with an
age-related rise in oxidative damage to DNA.
1 YEAR M PHARM ANSARI AASHIF RAZA
8
Alzheimer’s disease: Alzheimer's disease (AD) is under increased
oxidative stress and this may have a role in the pathogenesis of neuron
degeneration and death in this disorder.
The direct evidence supporting increased oxidative stress in AD is:
(1) increased in brain fe, al, and hg in AD, capable of stimulating free radical
generation
(2) increased lipid peroxidation and decreased polyunsaturated fatty acids in the
brain causes AD.
(3) Increased protein and DNA oxidation in the brain causes AD.
(4) diminished energy metabolism and decreased cytochrome c oxidase in the
brain
(5) that amyloid beta peptide is capable of generating free radicals. So free
radicals are possibly involved in the pathogenesis of neuron death in Alzheimer’s
disease (AD). 1 YEAR M PHARM ANSARI AASHIF RAZA 9
Parkinson's Disease:
Dopamine is metabolized in the cytosol and can result in the production of
hydrogen peroxide.
Increased dopamine turnover has been reported in the cytosol of patients
suffering from Parkinson's disease, which leaves them predisposed to higher
levels of hydrogen peroxide.
Hydrogen peroxide can be converted to highly reactive hydroxyl radicals
which are extremely toxic and can cause damage to dopaminergic neurons.
Increased lipid peroxidation, elevated iron levels, increased production of
ROS, and decreased levels of reduced glutathione have all been identified in
the substantia nigra of patients suffering from Parkinson's disease.
1 YEAR M PHARM ANSARI AASHIF RAZA
10
1 YEAR M PHARM ANSARI AASHIF RAZA
11

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AP 2 FREE RADICAL SEMINAR ANSARI AASHIF RAZA.pptx

  • 1. SUBJECT: ADVANCED PHARMACOLOGY –II GUIDED BY Dr. DEEPARANI UROLAGIN RR COLLEGE OF PHARMACY RR LAYOUT, CHIKKABANAVARA, BANGALORE 560090 PRESENTED BY ANSARI AASHIF RAZA (IInd semester , M.PHARM) DEPARTMENT OF PHARMACOLOGY FREE RADICALS PHARMACOLOGY 1 YEAR M PHARM ANSARI AASHIF RAZA 1
  • 2. Free radicals: • A free radical is defined as any chemical species that contains unpaired electron (s) in its outer orbit. INTRODUCTION 1 YEAR M PHARM ANSARI AASHIF RAZA 2
  • 3. • Atomic or molecular species with unpaired electrons on an otherwise open shell configuration. • These unpaired electrons are usually highly reactive, so radicals are likely to take part in chemical reactions. • Through a chain of oxidative reactions to cause tissue injury, like lipids, proteins, and nucleic acids, free radical damage is associated with oxidative damage, causing direct cellular injury by inducing lipid and protein peroxidation and damaging nucleic acids. 1 YEAR M PHARM ANSARI AASHIF RAZA 3
  • 4. FREE RADICALS A]Superoxide (O2 . -) B]Hydroxyl Radical (OH. ) C] Peroxyl ( R00. ) D]NO Physiological Stimuli that Form Free Radicals Normal respiration – • O2 – Superoxide, • H2O2 – Hydrogen Peroxide • HOCL – Hypochlorous acid • NO – Nitric Oxide Transition metals present inside our body when are in free form behave as free radicals. Fe2+, Cu+ 1 YEAR M PHARM ANSARI AASHIF RAZA 4
  • 5.  Pathological Stimuli that Form FRs Radiation →Breaks the water inside our body: H2O =H+ + OH- • Metabolism of drugs → CCl3 • Transition Metals → Cu+, Fe2+ • Ultraviolet rays • Emotional stress  Reactive Oxygen Species (ROS) • superoxide anion (O2 - ) • hydroxyl radical (·OH) • Hypochlorous acid ( HOCl) • Singlet Oxygen (1DgO2) - oxygen at an excited state • Hydrogen Peroxide (H2O2). H2O2 is considered a reactive oxygen species because of its ability to generate highly reactive hydroxyl free radicals through interactions with reactive transition metals Fe and Cu. 1 YEAR M PHARM ANSARI AASHIF RAZA 5
  • 6. REACTIVE OXYGEN SPECIES (ROS):  These are free radicals derived initially from oxygen. But as they do not contain unpaired electrons in their outermost orbit, they do not qualify as free radicals and so are referred to separately as ROS. E.g.- H2O2, HOCL, NO. Free radicals are formed inside our body by both PHYSIOLOGICAL (Natural) and PATHOLOGICAL stimuli. Role of ROS 1. important role in a number of physiological processes, including the intracellular killing of bacteria by neutrophil granulocytes detoxification by the liver 2. prostaglandin production and certain cell signaling processes 3. During the oxidative phosphorylation or one-electron reduction of O2 in the mitochondria (respiration) as the natural byproduct 1 YEAR M PHARM ANSARI AASHIF RAZA 6
  • 7. ROLE OF FREE RADICALS IN ETIOPATHOGENESIS o When produced in excess, free radicals and oxidants generate a phenomenon called oxidative stress, a deleterious process that can seriously alter the cell membranes and other structures such as proteins, lipids, lipoproteins, and DNA. o Oxidative stress results from an imbalance between the formation and neutralization of ROS/RNS. 1 YEAR M PHARM ANSARI AASHIF RAZA 7
  • 8. Cancer: Like radiation and carcinogens, free-radical oxidation breaks strands of DNA. The breaks are repaired, but some mistakes occur leading to mutations. These genetic mutations can cause cancers. The age-related increase in cancer rates might have something to do with an age-related rise in oxidative damage to DNA. 1 YEAR M PHARM ANSARI AASHIF RAZA 8
  • 9. Alzheimer’s disease: Alzheimer's disease (AD) is under increased oxidative stress and this may have a role in the pathogenesis of neuron degeneration and death in this disorder. The direct evidence supporting increased oxidative stress in AD is: (1) increased in brain fe, al, and hg in AD, capable of stimulating free radical generation (2) increased lipid peroxidation and decreased polyunsaturated fatty acids in the brain causes AD. (3) Increased protein and DNA oxidation in the brain causes AD. (4) diminished energy metabolism and decreased cytochrome c oxidase in the brain (5) that amyloid beta peptide is capable of generating free radicals. So free radicals are possibly involved in the pathogenesis of neuron death in Alzheimer’s disease (AD). 1 YEAR M PHARM ANSARI AASHIF RAZA 9
  • 10. Parkinson's Disease: Dopamine is metabolized in the cytosol and can result in the production of hydrogen peroxide. Increased dopamine turnover has been reported in the cytosol of patients suffering from Parkinson's disease, which leaves them predisposed to higher levels of hydrogen peroxide. Hydrogen peroxide can be converted to highly reactive hydroxyl radicals which are extremely toxic and can cause damage to dopaminergic neurons. Increased lipid peroxidation, elevated iron levels, increased production of ROS, and decreased levels of reduced glutathione have all been identified in the substantia nigra of patients suffering from Parkinson's disease. 1 YEAR M PHARM ANSARI AASHIF RAZA 10
  • 11. 1 YEAR M PHARM ANSARI AASHIF RAZA 11