cyanogenic glycosides and cardiac glycosides Flashcards Preview

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Flashcards in cyanogenic glycosides and cardiac glycosides Deck (8)
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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


cyanogylcoside biology

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


HCN poisoning

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


HCN symptoms

- 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


Cardiac glycoside

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


Cardiac mechanism

• 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


Cardiac symptoms

– 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)


Specific heart symptoms

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