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The energy-deprived state observed in hypoxic conditions can be compensated by the degradation of certain molecules containing high-energy phosphate bonds, leading to increased levels of adenosine, which is subsequently degraded to hypoxanthine, xanthine, and ultimately uric acid 49

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Studies at his laboratory led Goth to suggest that mutations of the CAT gene and resultant structural changes in the catalase protein are responsible for Hungarian acatalasemia

The ratio of reduced glutathione (GSH) to its oxidized form (GSSG) serves as a fundamental marker of the intracellular redox environment

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