1971
DOI: 10.1093/ajcn/24.4.444
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Metabolism of 14C- and 3H-labeled l-ascorbic acid in human scurvy

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1979
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Cited by 135 publications
(43 citation statements)
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“…118 The clinical features of vitamin C deficiency include follicular hyperkeratosis, inflamed and bleeding gums, perifollicular haemorrhages and impaired wound healing. 118,238,239 Deficiency in infants may result in bone abnormalities, such as impaired bone growth and disturbed ossification, haemorrhagic symptoms and resultant anaemia. 240 While scurvy is rare in modern societies (as previously discussed), subclinical vitamin C deficiency is relatively common even in affluent societies.…”
Section: Deficiencies: Relevance and Prevalencementioning
confidence: 99%
“…118 The clinical features of vitamin C deficiency include follicular hyperkeratosis, inflamed and bleeding gums, perifollicular haemorrhages and impaired wound healing. 118,238,239 Deficiency in infants may result in bone abnormalities, such as impaired bone growth and disturbed ossification, haemorrhagic symptoms and resultant anaemia. 240 While scurvy is rare in modern societies (as previously discussed), subclinical vitamin C deficiency is relatively common even in affluent societies.…”
Section: Deficiencies: Relevance and Prevalencementioning
confidence: 99%
“…Threshold urinary excretion of vitamin C was reported at the 60-mg daily dose (3,4,7,8 tTo whom reprint requests should be addressed.…”
Section: Introductionmentioning
confidence: 99%
“…The recommended dietary allowance (RDA) for vitamin C is 60 mg daily, based on threshold urinary excretion of the vitamin and on preventing the vitamin C deficiency disease scurvy with a margin of safety (1,2).. Ingestion of 60 mg daily was proposed to prevent scurvy for [30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45] days if vitamin C intake ceased (1)(2)(3)(4)(5)(6)(7). Threshold urinary excretion of vitamin C was reported at the 60-mg daily dose (3,4,7,8).…”
Section: Introductionmentioning
confidence: 99%
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“…In a rat model of chronic ethanol ingestion, this altered GSH homeostasis in the ELF (14) resulted in increased susceptibility to sepsis-induced acute lung injury as well as impaired alveolar type II cell function and viability (1,5,12). An important role for GSH availability as a predisposing factor to the development of acute lung injury was demonstrated by the ability of GSH precursors to attenuate injury in the rat model (4,5,14).…”
mentioning
confidence: 99%