Galactosemia caused by a transferase deficiency is characterized by elevated levels of galactose, galactitol, and galactose 1‑ph
osphate. Galactose and galactitol are precursors of galactose 1‑phosphate. Transferase deficiency studies in animal models suggest that galactose 1‑phosphate is the toxic agent. Which result from a galactosemia study in an animal model will implicate galactose 1‑phosphate as the toxic agent in a transferase deficiency? Inhibition of UDP‑glucose 4‑epimerase in affected animals prevents toxicity. Affected animals given a lactase inhibitor do not experience toxicity. Inhibition of galactose transporter in the intestinal cells prevents toxicity. Affected animals given a galactokinase inhibitor do not experience toxicity. A galactose‑free diet eliminates toxicity in affected animals.
Affected animals given a galactokinase inhibitor do not experience toxicity.
Explanation:
Galactokinase: Catalyzes is the first and committed step of the Leloir pathway involving the conversion of galactose to glucose. It causes phosphorylation of α-D-galactose to galactose 1‑phosphate. Thus, inhibiting galactokinase wil greatly decrease the levels of galactose 1‑phosphate.
The formation of a gas is a clue to chemical changes. The bubbles of gas that you observed form when an antacid is dropped into water is an example of change. ... After ice melts into liquid water, you can refreeze it into solid ice if the temperature drops. Freezing and melting are physical changes.
This is because the cell membrane is a partially permeable membrane, hence allowing the smaller molecules to enter it and larger molecules to be out. For example, protein is too large to enter the cell
