Measurement of ascorbic acid in human plasma and urine by high-performance liquid chromatography results in healthy subjects and patients with idiopathic calcium urolithiasis

Manoharan, M.; Schwille, P. O.

doi:10.1016/0378-4347(94)00008-5

Cited by 13 publications

(1 citation statement)

References 13 publications

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“…High pressure liquid chromatography (HPLC) was used for the determination of vitamin C according to the technique described by Manoharan and Schwille [29]. First, 100 µL of 10% perchloric acid mixed with 1% metaphosphoric acid were added to 200 µL of plasma or erythrocytes, stirred in a vortex for 30 s and stored in a refrigerator for 20 min.…”

Section: Nonenzymatic Antioxidant Determinationmentioning

confidence: 99%

Association between Parameters Related to Oxidative Stress and Trace Minerals in Athletes

et al. 2020

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The aim of the present study was to evaluate the basal concentrations of malondialdehyde (MDA) nonenzymatic antioxidants, such as ascorbic acid, α-tocopherol, and retinol in plasma or erythrocytes, and the plasma concentrations of 16 trace minerals in endurance athletes from Extremadura (Spain). In addition, we aimed to assess the possible relationships between some parameters related to cellular oxidative stress with plasma concentrations of some trace minerals. Sixty-two national long-distance men athletes participated in this study. The parameters related to oxidative stress and antioxidant activity were analyzed through high pressure liquid chromatography (HPLC), and trace minerals analysis was performed by inductively coupled plasma mass spectrometry (ICP-MS). We found that plasma MDA was positively correlated with selenium and rubidium. Plasma ascorbic acid was positively correlated with manganese and negatively correlated with cobalt and cadmium. Erythrocyte ascorbic acid was related to arsenic and cesium. Plasma α-tocopherol correlated with copper and manganese negatively and positively with arsenic. Erythrocyte α-tocopherol was positively related to copper, rubidium, and lithium. The findings show that athletes with a high degree of training should monitor their intake and concentrations of α-tocopherol for its fundamental role of neutralizing the excess of reactive oxygen species produced by exercise and the prooxidant effects of several minerals such as arsenic, copper, and lithium.

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Section: Nonenzymatic Antioxidant Determinationmentioning

confidence: 99%

Association between Parameters Related to Oxidative Stress and Trace Minerals in Athletes

et al. 2020

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Postprandial hyperinsulinaemia, insulin resistance and inappropriately high phosphaturia are features of younger males with idiopathic calcium urolithiasis: Attenuation by ascorbic acid supplementation of a test meal

et al. 1997

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In idiopathic recurrent calcium urolithiasis (RCU) the state of insulin and carbohydrate metabolism, and relationships to minerals such as phosphate, are insufficiently understood. Therefore, in two groups of males with RCU (n = 30) and healthy controls (n = 8) the response to an oral carbohydrate- and calcium-rich test meal was studied with respect to glucose, insulin, and C-peptide in peripheral venous blood (taken before and up to 180 min post-load), and phosphate and glucose in fasting and post-load urine. In one RCU group (n = 16) the meal was supplemented with ascorbic acid (ASC; 5 mg/kg body weight). The mean age (RCU 29, RCU + ASC 30, controls 27 years) and mean body mass index [RCU 24.4, RCU + ASC 25.0, controls 24.0 kg/m2] were similar. Insulin resistance (synonymous sensitivity of peripheral organs to insulin) was calculated from insulin serum concentration, as was also integrated insulin, C-peptide, and glucose. Untreated stone patients (RCU) developed hyperinsulinaemia between 60 and 120 min post-load, increased integrated insulin, and insulin resistance (P < or = 0.05 vs controls), whereas the rise of C-peptide and glycaemia (absolute and integrated values) was only of borderline significance. Fasting phosphaturia was low in both RCU subgroups vs controls; however, phosphaturia in untreated RCU rose in response to the meal, contrasting sharply with a decrease in controls. ASC supplementation of the meal (in the RCU + ASC subgroup) normalized insulin, failed to normalize post-load phosphaturia, but reduced post-load glucosuria and urinary pH significantly (mean pH values 5.55 vs 5.93 in untreated RCU, controls 5.50). Postprandial urinary oxalate, calcium, protein, and supersaturation products were not changed. The postprandial changes in phosphaturia and insulin sensitivity were inversely correlated (n = 38, r = -0.44, P = 0.007). It was concluded that in younger RCU males: (1) postprandial hyperinsulinaemia, the failure to reduce phosphaturia and - within limits - glucosuria, appropriately, as well as poor urine acidification are important features of the metabolism; (2) these phenomena are probably caused by insulin resistance of organs, the kidney included; and (3) the addition of a supraphysiological dose of ASC to a meal, the subsequent abolition of hyperinsulinaemia, and the restoration of normal urine acidification suggest that this antioxidant is capable of counteracting some pre-existing basic abnormality of cell metabolism in RCU.

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Ascorbic acid in idiopathic recurrent calcium urolithiasis in humans - does it have an abettor role in oxalate, and calcium oxalate crystallization?

Schwille

Schmiedl

Herrmann

et al. 2000

Urological Research

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The role of ascorbic acid (ASC) in the pathophysiology of renal calcium stones is not clear. We evaluated ASC in blood and urine of fasting male patients with idiopathic calcium urolithiasis (ICU) and healthy volunteers. Using smaller subgroups, we also evaluated their response to exogenous ASC [either intravenous or oral ASC (5 mg/kg bodyweight)] administered together with an oxalate-free test meal. The influence of ASC on calcium oxalate crystallization, the morphology of crystals at urinary pH 5, 6 and 7, and the effect of increasing duration of urine incubation on urinary oxalate at these pHs, without and with addition of ASC, were studied too. In normo- and hypercalciuric ICU, blood and urinary ASC from fasting patients remained unchanged, but the slope of the regression line of urinary ASC versus urinary oxalate was steeper than in the controls; the plasma ASC half-life did not differ between controls, normo- and hypercalciuric ICU; the ASC-supplemented meal caused an increase in the integrated plasma oxalate in the normocalciuric subgroup versus controls. In normo- and hypercalciuric ICU urinary oxalate, the oxalate/glycolate ratio, and calcium oxalate supersaturation were increased, but urinary glycolate was unchanged. In the controls, oral ASC did not affect calcium oxalate crystallization, while in ICU, ASC inhibited crystal growth. In control urine calcium oxalate dihydrate and calcium oxalate monohydrate develops, while in ICU urine only the former crystal type develops. In vitro oxalate neoformation from ASC did not occur. It was concluded that (1) under normal conditions an abettor role of ASC for renal stones is not recognizable, (2) in ICU, urinary oxalate excess unrelated to degradation of exogenous ASC is exhibited, and that this is most likely unrelated to an initial increase in oxalate biosynthesis, and (3) ASC appears to modulate directly calcium oxalate crystallization in ICU, although the true mode of action is still not known.

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Measurement of ascorbic acid in human plasma and urine by high-performance liquid chromatography results in healthy subjects and patients with idiopathic calcium urolithiasis

Cited by 13 publications

References 13 publications

Association between Parameters Related to Oxidative Stress and Trace Minerals in Athletes

Association between Parameters Related to Oxidative Stress and Trace Minerals in Athletes

Postprandial hyperinsulinaemia, insulin resistance and inappropriately high phosphaturia are features of younger males with idiopathic calcium urolithiasis: Attenuation by ascorbic acid supplementation of a test meal

Ascorbic acid in idiopathic recurrent calcium urolithiasis in humans - does it have an abettor role in oxalate, and calcium oxalate crystallization?

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