ArticleBiochimica et biophysica acta2016
Effects of alanine:glyoxylate aminotransferase variants and pyridoxine sensitivity on oxalate metabolism in a cell-based cytotoxicity assay.
Article in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- SGLT2 Inhibitors in Nephrolithiasis: Emerging Evidence and What Urologists Need to Know.Medical sciences (Basel, Switzerland) · 2026Review
- 4-hydroxy-2-oxoglutarate metabolism in a mouse model of Primary Hyperoxaluria Type 3.Biochemistry and biophysics reports · 2024Article
- Infant primary hyperoxaluria type 1Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- Vitamins as regulators of calcium-containing kidney stones - new perspectives on the role of the gut microbiome.Nature reviews. Urology · 2023Review
- Clinical and molecular characterization of a large primary hyperoxaluria cohort from Saudi Arabia: a retrospective study.Pediatric nephrology (Berlin, Germany) · 2023Article
- Physiological Associations between Vitamin B Deficiency and Diabetic Kidney Disease.Biomedicines · 2023Review
- Identification of Human Alanine-Glyoxylate Aminotransferase Ligands as Pharmacological Chaperones for Variants Associated with Primary Hyperoxaluria Type 1.Journal of medicinal chemistry · 2022Article
- Generation of a GLO-2 deficient mouse reveals its effects on liver carbonyl and glutathione levels.Biochemistry and biophysics reports · 2021Article
- Dual Glycolate Oxidase/Lactate Dehydrogenase A Inhibitors for Primary Hyperoxaluria.ACS medicinal chemistry letters · 2021Article
- Recovery From Dialysis in Patients With Primary Hyperoxaluria Type 1 Treated With Pyridoxine: A Report of 3 Cases.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2021Article
- Effect of alanine supplementation on oxalate synthesis.Biochimica et biophysica acta. Molecular basis of disease · 2021Article
- The effects of the inactivation of Hydroxyproline dehydrogenase on urinary oxalate and glycolate excretion in mouse models of primary hyperoxaluria.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- Reduction in urinary oxalate excretion in mouse models of Primary Hyperoxaluria by RNA interference inhibition of liver lactate dehydrogenase activity.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- Translation inhibition corrects aberrant localization of mutant alanine-glyoxylate aminotransferase: possible therapeutic approach for hyperoxaluria.Journal of molecular medicine (Berlin, Germany) · 2018Article
- Molecular therapy of primary hyperoxaluria.Journal of inherited metabolic disease · 2017Review
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The hereditary kidney stone disease primary hyperoxaluria type 1 (PH1) is caused by a functional deficiency of the liver-specific, peroxisomal, pyridoxal-phosphate-dependent enzyme, alanine:glyoxylate aminotransferase (AGT). One third of PH1 patients, particularly those expressing the p.[(Pro11Leu; Gly170Arg; Ile340Met)] mutant allele, respond clinically to pharmacological doses of pyridoxine. To gain further insight into the metabolic effects of AGT dysfunction in PH1 and the effect of pyridoxine, we established an "indirect" glycolate cytotoxicity assay using CHO cells expressing glycolate oxidase (GO) and various normal and mutant forms of AGT. In cells expressing GO the great majority of glycolate was converted to oxalate and glyoxylate, with the latter causing the greater decrease in cell survival. Co-expression of normal AGTs and some, but not all, mutant AGT variants partially counteracted this cytotoxicity and led to decreased synthesis of oxalate and glyoxylate. Increasing the extracellular pyridoxine up to 0.3μM led to an increased metabolic effectiveness of normal AGTs and the AGT-Gly170Arg variant. The increased survival seen with AGT-Gly170Arg was paralleled by a 40% decrease in oxalate and glyoxylate levels. These data support the suggestion that the effectiveness of pharmacological doses of pyridoxine results from an improved metabolic effectiveness of AGT; that is the increased rate of transamination of glyoxylate to glycine. The indirect glycolate toxicity assay used in the present study has potential to be used in cell-based drug screening protocols to identify chemotherapeutics that might enhance or decrease the activity and metabolic effectiveness of AGT and GO, respectively, and be useful in the treatment of PH1.
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