Basic Aspects of Biochemistry: Amino Acids, Proteins, Enzyme Kinetics Flashcards
normal PH range of arterial blood
7.37-7.43
Hydrophobic amino acids with aliphatic side group:
V, L, I, G, A, P.
Draw the reaction dissociation of 7 ionizable aa’s at PH below and above the PKa’s: D (PKa= 3.9) E (4.1) H (6.0) C (8.4) Y (10.5) K (10.5) R (12.5)
Ionizable groups on amino acids carry protons at low pH (high [H+]), which dissociate as
the pH increases. If the pH is below an ionizable group’s pKa, then the group will be protonated.
Once the pH is above the pKa, the group will be deprotonated.
two major causes of resp. acidosis
accumulation of metabolic acids and ingestion of comp that metblz 2 acid
Structure of R at PH< Pka
Y
TYR, PKa= 8.4
lungs and kidneys compensatory behavior during METABOLIC ACIDOSIS
met. acidosis –> hypERventilation and the release of CO2. The kidneys excrete NH4+, which contains H+ buffered by ammonia
relatively more polar aromatic amino acid
Tyr, Y > Trp, W
Structure of R at PH< Pka
H
HIS
PKa= 6.0
7 amino acids with ionizable groups and the corresponding PKa’s:
Asp 3.9 Glu 4.1 His 6.0 Cys 8.4 Tyr 10.5 Lys 10.5 Arg 12.5
Causes metabolic alkalosis
inc. HCO3-
Structure of R at PH< Pka C
CYS PKa= 8.4
causes the retention of CO2 by the lungs and leads to a respiratory acidosis
hypOventilation
name a few acidic comps that can cause metabolic acidosis upon their accumulation
1- lactic acid 2- ketone bodies:(B-hydrozybutyrate and acetoacetate) 3- B-hydroxybutyric acid 4- acetoacetic acid
hupOventilation (acid-base disturbance)
respiratory acidosis due to CO2 retention by the lungs
purpose of drugs that inhibit H+/K+ ATPase of parietal cells
to lower the [H+] (inc. the PH of stomach content and to lessen the esophageal damage ( when gastroesophageal sphincter fails to close, gastric reflux disease occurs).
Structure of R at PH< Pka
E
GLU
- CH2-CH2-COOH
- (CH2)2-COOH
PKa= 4.1
The max capacity of a buffer
At the PKa,whete [A-] and [HA] are equal the buffer has its max capacity.
NH4+ and Acid-Base disturbance
When metabolic acidosis –> kidneys excrete H+ buffered by ammonia (NH3)
The compounds that upon digestion cause metabolic acidosis
These comps results in accumulation of acid upon digestion: methanol, ethylene glycol
W
Trp
hypERventilation (acid-base disturbance)
resp. alkalosis
Positively charged amino acids are:
basic Arg, R Lys, K His, H
Henderson–Hasselbalch equation
pH = pK + log10 [A−]/ [HA]
sulfhydryl oxidation
form disulfide
The amino acid that is NOT of L-configuration and dose NOT have Asymmetric a-carbon:
glycine.
Structure of R at PH< Pka K
K LYS
PKa= 10.5
selenocysteine
unique aa in that a serine residue is converted to selenocysteine while attached to a tRNA.
Negatively charged amino acids are:
acidic Asp, D- Aspartate Glu, E- Glutamate
sulfur-containing amino acids
Met, M Cys, C
Structure of R at PH< Pka
R
ARG, PKa= 12.5
Non-polar aromatic amino acid
Phe, P
Polar, uncharged amino acids
Asn,N (aspargine) Gln, Q (glutamine) Ser, S (hydroxyl group) Thr, T (hydroxyl group)
- Name two major buffers of blood?
- How do they work in conjugation with other organs to maintain the normal PH?
- Major buffers:
- Bicarbonate (HCO3-/H2CO3)
- Hemoglobin (Hb/HHb)
- Organs:
- Kidney- excreting protons
- Lung- CO2 exchange
Structure of R at PH< Pka
D
Asp
-CH2-COOH
PKa= 3.9
Amino acids capable of hydrogen bonding:
T, S.