cyanogenic glycosides and cardiac glycosides Flashcards

1
Q

cyanoglycoside

A

A glycoside is a molecule in which a sugar is bound to another functional group via a glycosidic bond

The sugar group is then called glycone and the non- sugar part is aglycone

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2
Q

cyanogylcoside biology

A

CGs are produced from amino acids

In plant tissues, CGs are stored in vacuola in inactive forms

  • Upon plant injury, specific enzymes remove the sugar parts
  • Aglycones are activated; HCN is often produced spontaneously
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3
Q

HCN poisoning

A

In animals, HCN can easily enter the tissues via mucous membranes (from respiratory system and gastrointestinal tract), or from skin surface

HCN inhibits cytochrome C oxidase enzyme (the last enzyme in the respiratory electron transport chain located in the mitochondrial membrane) inhibition of cellular respiration —> no more ATP (energy) is produced –> death

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4
Q

HCN symptoms

A
  • blood, mucous membranes (and skin) of cherry colour; clotting of blood is slow
  • nausea, vomiting, breath with smell of bitter almond - heavy breathing
  • muscle contraction, spasms
  • stumbled walk, coma, death
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5
Q

Cardiac glycoside

A

In cardiac glycosides the aglycone is a steroid

  • Both in animals and plants, steroid skeleton is biosynthesised from squalene (one of the most important triterpene)
  • Aglycones in cardiac glycosides can be classified into three groups: cardenolides, bufadienolides, and steroidal sapogenins
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6
Q

Cardiac mechanism

A
  • Na+/K+ pumps in cell membranes are inhibited increased Na+ levels within cardiac muscle (CM) cells
  • Na+/Ca2+ exchangers (NCX, responsible for pumping Ca2+ out of the CM cell and Na+ in) got inhibited also due to the raised levels of intracellular Na+ –> raised Ca2+ levels in CM cells
  • Increased cytoplasmic Ca2+ levels cause increased Ca2+ uptake into the sarcoplasmic reticulum (SR)
  • Raised Ca2+ stores in the SR allow for a greater Ca2+ release on stimulation, so the (CM) cells can achieve faster and more powerful contractions (positive inotropic effect) decreased heart rate (negative chronotropic effect)
  • Slow catabolism of cardiac glycosides
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7
Q

Cardiac symptoms

A

– nausea, vomiting, disorders of color vision, hallucinations

– decreased heart rate, cardiac arrhythmias, tremor, seizures, coma, death

• Low K+ level in blood higher affinity of the toxin to bind to the ATP-pump (due to phosohorylation)

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8
Q

Specific heart symptoms

A
  • acute heart failure
  • ST depression
  • myocardial damages the electrical conduction system of heart is affected
  • increased heart rate, weak pulse, irregular heartbeat
  • death
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