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Alekssandra [29.7K]
4 years ago
10

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.
Biology
1 answer:
vova2212 [387]4 years ago
6 0

Answer:

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.

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Answer:

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In short, the glucose splits by glycolysis and produces ATP, NADPH, and final product pyruvate. The pyruvate is oxidized and forms acetyle coenzyme. This is used in the TCA / citric acid cycle. In this process also NADH, FADH2 which forms electrons are produced. Theses electrons are carried by different electron carriers and accepted by oxygen.

In the process of pyruvate oxidation 6 ATP, and in Kreb's cycle 18 ATPs, in ETS, 4 ATPs are produced. In addition to this in glycolysis produces 4 ATPs. The total number of ATP in aerobic respiration is 32 ATP.  

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