Abstract
Sodium benzoate (SB) therapy in hyperammonemic children is based on the elimination of excess nitrogen as hippurate, but its mechanism is speculatory. We gave 2 % SB in drinking water to normal (+/Y) and spf/Y mice. After acclimatization for 48 h, i.p. 3H-glycine and 14C-serine were given as sources of transported and biosynthesized glycine respectively. 24 h urine was analyzed for total hippurate, free glycine and orotate. Hippurate spots were separated by TLC and counted for radioactivity. Output of hippurate and free glycine increased significantly in SB treated spf/Y and +/Y as compared to untreated mice, while orotate excretion decreased (p < 0.013). Specific activity of 3H and 14C (DPM/μmol hippurate) showed significant increases in treated groups, indicating utilization of transported and biosynthesiged glycine. However, 3H;14C ratio showed predominant use of 3H-glycine. The ratio was higher in treated spf mice as compared to untreated controls (3.1 ± 0.7 Vs 1.5 ± 0.04; p < 0.02); same increase was seen in +/Y (1.9 ± 0.2 Vs 1.0 ± 0.1; p <0.01). The results indicate that transported glycine has a bigger contribution in the formation of hippurate in vivo than glycine synthesized from serine. Since glycine is highly ammoniagenic, we postulate that the conjugation of excess glycine transported from body pools would result in depletion of ammoniagenic potential. This would be supplemented by the effect of glycine biosynthesis through reactions requiring a metabolic input of NH3.
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