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Redox never been intuitive to me, so for the millionth time...
REDUCTION is the GAIN of electrons by an atom. By gaining electrons (becoming more negatively charged) it is reduced.
The electrons derive from a REDUCING AGENT, which in the process becomes oxidized.
REDUCTION is the GAIN of electrons by an atom. By gaining electrons (becoming more negatively charged) it is reduced.
The electrons derive from a REDUCING AGENT, which in the process becomes oxidized.
OXIDATION is the LOSS of electrons from an atom. By losing electrons (becoming more positively charged) it is oxidized.
An OXIDIZING AGENT accepts the electrons, and in the process, is reduced.
An OXIDIZING AGENT accepts the electrons, and in the process, is reduced.
Example: the oxidation of ferrous (Fe2+) iron in hemoglobin to ferric (Fe3+) iron results in methemoglobin.
The metabolism of ethanol is another example. Ethanol undergoes oxidation to acetaldehyde (by ADH), which then is oxidized further (by ALDH) to acetate (then off to Krebs cycle, yada yada CO2 and H20)
In this case, ADH oxidizes (removes electrons from) the C-O bond and delivers those electrons to the oxidizing agent (electron acceptor) NAD+
NAD+ is the oxidizing agent in this reaction. It accepts electrons.
NAD+ is the oxidizing agent in this reaction. It accepts electrons.
NAD = nicotinamide adenine dinucleotide
This co-factor, central to all of metabolism, exists in two forms: oxidized (NAD+) and reduced (NADH)
This co-factor, central to all of metabolism, exists in two forms: oxidized (NAD+) and reduced (NADH)
Conversely, the reduced form (NADH) is used in the generation of ATP.
In this instance, it is a reducing agent.
It donates electrons to the oxidative phosphorylation cascade.
In this instance, it is a reducing agent.
It donates electrons to the oxidative phosphorylation cascade.
Part of the pathophysiology of alcoholic ketoacidosis (AKA) is that in the course of metabolizing large amounts of ethanol, there is excessive production of NADH (and not enough NAD+)
In AKA, there is an excess of reducing agents (NADH), and a paucity of oxidizing agents (NAD+)
In AKA, there is an excess of reducing agents (NADH), and a paucity of oxidizing agents (NAD+)
While at first one might think "great, more NADH = more ATP = more energy" the redox imbalance creates metabolic problems. We see these in AKA.
The end product of glycolysis is pyruvate, which normally enters the Krebs cycle to create ATP.
In anaerobic metabolism, however, pyruvate is reduced to lactate. In this reaction, NADH is the reducing agent.
NADH donates electrons to pyruvate to make lactate.
In anaerobic metabolism, however, pyruvate is reduced to lactate. In this reaction, NADH is the reducing agent.
NADH donates electrons to pyruvate to make lactate.
With the redox imbalance from AKA (too much reducing power), this reaction is favored and pyruvate is excessively converted to lactate.
Thus the accompanying "lactic acidosis" seen sometimes in AKA is driven (somewhat) by the redox imbalance inherent to metabolizing ethanol.
Thus the accompanying "lactic acidosis" seen sometimes in AKA is driven (somewhat) by the redox imbalance inherent to metabolizing ethanol.
This does not account for the ketosis part, however.
Acetyl-CoA accumulates, both from acetate and from fatty acid oxidation. Acetyl-CoA combines with excess acetate (also from ethanol metabolism) to create acetoacetate.
Acetoacetate exists in redox equilibrium with...
Acetyl-CoA accumulates, both from acetate and from fatty acid oxidation. Acetyl-CoA combines with excess acetate (also from ethanol metabolism) to create acetoacetate.
Acetoacetate exists in redox equilibrium with...
...beta-hydroxybutyrate (BHB).
Acetoacetate is reduced to BHB. The redox imbalance in AKA favoring reducing power (
NADH:NAD+ ratio) favors the conversion of acetoacetate to BHB.
In this case the reducing agent is NADH; it donates electrons to acetoacetate to become BHB
Acetoacetate is reduced to BHB. The redox imbalance in AKA favoring reducing power (
NADH:NAD+ ratio) favors the conversion of acetoacetate to BHB. In this case the reducing agent is NADH; it donates electrons to acetoacetate to become BHB
When you measure a "serum ketones" in a patient, what you measure is BHB.
Hence the high anion-gap metabolic acidosis of AKA is sometimes (in part) a "lactic" acidosis, but always is a ketoacidosis.
Hopefully writing this out helps it stick in my brain for the next 6 weeks...
Hence the high anion-gap metabolic acidosis of AKA is sometimes (in part) a "lactic" acidosis, but always is a ketoacidosis.
Hopefully writing this out helps it stick in my brain for the next 6 weeks...
