OZONE THERAPYThe Role of Oxygen in Metabolism

BIOCHEMISTRY IS ORGANIC CHEMISTRY Occurs in living tissues and with a more finite array

of reactions. A few of those to be addressed here:

Acid + Alcohol -------------------------------> Ester + HOH

HYDROLYSIS = “splitting via water”

Condensation = combining two reactants and excluding HOH

Transamination = transferring and amine (-NH2) from one carbon chain to another

Deamination = removal of the -NH2 from a carbon chain

REDOX = Oxidation-Reduction (very important in cellular respiration)

De-carboxylation = removal of CO2 from the carboxyl group of an organic acid

HOH

GUIDE TO REACTION SYMBOLS

Hydrolysis

Condensation (dehydration)

Carboxylation

De-carboxylation

Oxidation

Reduction

[ HOH ]

HOH

CO2

CO2

[ O ]

THE SPEED (AND/OR) DIRECTION OF A BIOLOGICAL REACTION

may be influenced by any one, or a combination, of the following: Temperature

pH (H+ conc.)

Enzymes involved

Metabolic requirement of the cell

Concentration of substrate

Nature of the SUBSTRATE and REACTANTS

TERMINOLOGY AND SYNONYMS:

EMDEN-MEYERHOFF = EM = GLYCOLYSIS (occurs in the cytosol) Reducing agent is oxidized

KREBS CYCLE = CITRIC ACID CYCLE = Tricarboxylic acid (TCA) cycle (occurs in the matrix of the mitochondria)

ELECTRON TRANSPORT SYSTEM = ETS (occurs in the inner-mitochondrial membrane)

KEEP IN MIND:

Glycolysis occurs in the cytosol

TCA occurs in the mitochondrial matrix

Overall process (RESPIRATION) is influenced by:

Availability of substrate Metabolic requirements of cell (Demands of the

TCA) AVAILABILITY OF OXYGEN

GLYCEROL, FATTY ACIDS, AND TRIGLYCERIDES

ESTERIFICATION REACTION

KETOSIS

Acetone

Acetoacetic Acid

Beta Hydroxyl Butyric Acid (ketogenic)

Accumulation of KETONE BODIES as a result of incomplete fat metabolism and oxygen deficit. The Primary KETONE BODIES associated with KETOSIS:

REDOX REACTIONS ALWAYS PROCEED TOGETHER:

Oxidizing agent is reduced

Reducing agent is oxidized

VARIOUS EXPRESSIONS OF OXIDATION AND REDUCTION

Loss of electrons Addition of oxygen Gain of Protons Loss of H+ ions

Gain of electrons Loss of oxygen Loss of Protons Gain of H+ ions

OXIDATION REDUCTION

REDOX EXAMPLE

Oxidation of an alcohol to an acid and the reduction of an acid to an alcohol. (Aldehydes are intermediate products of the reaction)

TCA - FUNCTIONS IN THE MITOCHONDRIAL MATRIX

CO2 diffuses out as a waste

H+ diffuses to the inner-membrane space

Electrons (e- ) passed along ETS to molecular oxygen

ACETYL COA ENTERS THE TCA AND OXIDIZED COMPLETELY

CO2 - diffuses out

Electrons - ETS

H+ - inner-membrane space

WHEN THE ENERGY DEMANDS FOR WORK BECOME SO GREAT THAT THE OXYGEN SUPPLY CANNOT KEEP PACE:

NADH is “loaded” and has no place to “un-load” (H+ accumulate)

Buffer systems can regulate pH up to a point

Eventually the ANAEROBIC THRESHHOLD will be reached

From this point the body goes into OXYGEN-DEBT (pyruvate becomes an H+ acceptor)

THE OXIDATION OF LACTIC ACID AND REDUCTION OF PYRUVIC ACID

IONIZATION OF AN ORGANIC ACID

WHEN THE CAPACITY TO FORM LACTATE (IONIZED FORM OF LACTIC) IS EXCEEDED:

Buffer system overwhelmed

H+ accumulate

Enzyme systems cease ----- outside their optimum pH

NAD+ is reduced to NADH (has no electrical charge)

NAD+ (“pack mule”) becomes limiting

“PACK MULES” (NAD+ NADP+ FAD+) transport cargo (H+) to the ETS

They must “unload” to remain useful to the NAD+/NADH ratio

NOW -- ONCE WORK ABATES AND OXYGEN BECOMES AVAILABLE Liver converts lactic back to pyruvic (oxidation)

NADH can unload and become available to “reload”

H+ accumulation is reversed

pH drop is averted (acidosis avoided)

ATP formed from ADP

Energy is conserved

IF OXYGEN IS AVAILABLE (BY WHATEVER MEANS):

Pyruvate enters the mitochondria and is decarboxylated

Acetate (2-C) is picked up by CoAsH to form Acetyl-CoA then to TCA

ELECTRON TRANSFER SYSTEM (ETS)

Designed to SLOW THE FALL of electrons (e-) to oxygen via SEVERAL Redox reactions rather than ONE VIOLENT REACTION

THE ROLE OF PEROXIDASES IN THE ETS

(Preventing the accumulation of hydrogen peroxide)

ADENOSINE TRI-PHOSPHATE (ATP)

FORMATION OF AN ACID ANHYDRIDE BOND

INCREASING THE AVAILABILITY OF OXYGEN:

Accelerates the regeneration of NAD+ (therefore recovery time)

Regeneration of ATP

Multitude of anabolic effects

SUMMARY AND CONCLUSIONS:

Based on the foregoing discussion ---- it seems logical to assume that—

Any mechanism which can enhance the availability of OXYGEN to the cell would:

Delay the ANAEROBIC THRESHHOLD and the point of oxygen debt

Reduce the stress on the cells BUFFER SYSTEM Reduce the wasteful loss of energy from the

initial dietary source of carbon and hydrogen Maintain the availability of NAD+ and therefore,

improve the NAD+ / NADH ratio Enhance the healing and recovery process in

cases of injury or illness