Vitamin A Antagonizes Calcium Response to Vitamin D in Man

Johansson, Sandra; Melhus, Håkan

doi:10.1359/jbmr.2001.16.10.1899

Cited by 150 publications

(87 citation statements)

References 39 publications

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“…An effect of retinoids on calcium homeostasis has been shown more clearly in studies investigating the association between vitamin A and fracture risk, [45][46][47][48] and the influence of retinoids on vitamin D regulation of serum calcium and bone mineral homeostasis. 35,49,50 Unfortunately, we were unable to obtain sufficient data to report serum or urine calcium levels in our study. Metabolic cages were not used in this study, and urine collections did not provide sufficient volume to perform urine calcium measurements in all pertinent groups.…”

Section: Discussionmentioning

confidence: 95%

Inhibition of lung carcinogenesis by 1α,25‐dihydroxyvitamin D₃ and 9‐cis retinoic acid in the A/J mouse model: Evidence of retinoid mitigation of vitamin D toxicity

Mernitz

Smith

Wood

et al. 2007

Intl Journal of Cancer

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9-cis-Retinoic acid (9cRA) and 1a, 25-dihydroxyvitamin D 3 (1,25D) show promise as potential chemopreventive agents. We examined 9cRA and 1,25D, alone and in combination, for their potential to inhibit carcinogen (NNK)-induced lung carcinogenesis in A/J mice. A/J mice (n 5 14/group) were treated with 9cRA (7.5, 15, or 30 mg/kg diet), 1,25D (2.5 or 5.0 lg/kg diet), or a combination of 9cRA (15 mg/kg diet) plus 1,25D (2.5 lg/kg diet) for 3 weeks before and 17 weeks after carcinogen injection. Lung tumor incidence, tumor multiplicity, plasma 1,25D levels and kidney expression of vitamin D 24-hydroxylase (CYP24) were determined. Compared to carcinogen-injected controls, mice receiving 9cRA supplementation had significantly lower tumor multiplicity at all doses (decreased 68-85%), with body weight loss at the higher doses of 9cRA. Mice receiving 1,25D supplementation had significantly lower tumor incidence (decreased 36 and 82%) and tumor multiplicity (decreased 85 and 98%), but experienced significant body weight loss, kidney calcium deposition, elevated kidney CYP24 expression and decreased fasting plasma 1,25D levels. Although, there was no apparent influence on chemopreventive efficacy, addition of 9cRA to 1,25D treatment effectively prevented the weight loss and kidney calcification associated with 1,25D treatment alone. These data demonstrate that 9cRA and 1,25D, alone or combined, can inhibit lung tumor promotion in the A/J mouse model. Combining 1,25D with 9cRA has the potential to mitigate the toxicity of 1,25D, while preserving the significant effect of 1,25D treatment against lung carcinogenesis. The underlying mechanism behind this effect does not appear to be related to retinoid modulation of vitamin D catabolism. ' 2006 Wiley-Liss, Inc.Key words: lung cancer; 9-cis retinoic acid; 1a,25-dihydroxyvitamin D 3Chemoprevention by diet or drug intervention may offer a realistic and practical means of modifying the risk of lung cancer, the leading cause of cancer deaths in both men and women in the United States. 1 Two classes of chemopreventive compounds that have been considered are the retinoids and the active form of vitamin D, 1a,25-dihydroxyvitamin D 3 (1,25D, also calcitriol).Retinoids are required for proper differentiation of lung and upper airway epithelium, 2 and both 9-cis retinoic acid (9cRA, also 9-cis tretinoin) and all-trans retinoic acid have been shown to inhibit cell growth and proliferation in lung cancer cell lines. 3 Studies in animal models of lung cancer suggest that retinoids may be effective in cancer chemoprevention in vivo, but results have varied with species, dose and timing of treatment in relation to induction of carcinogenesis. [4][5][6] In human lung cancer, epidemiological evidence supports a role for vitamin A-rich foods and supplements in protection against the development of lung cancer in smokers and nonsmokers alike 7 ; however, clinical trials assessing the efficacy of retinoid supplementation against lung cancer have yielded inconsistent and inconclusive results. [8][...

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Section: Discussionmentioning

confidence: 95%

Inhibition of lung carcinogenesis by 1α,25‐dihydroxyvitamin D₃ and 9‐cis retinoic acid in the A/J mouse model: Evidence of retinoid mitigation of vitamin D toxicity

Mernitz

Smith

Wood

et al. 2007

Intl Journal of Cancer

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“…Our results are consistent with those reported by El-Morsy et al (31), who referred to the protective effect of vitamin K in hypervitaminosis D 3 and the lack of any known toxic adverse effects from the use of large amounts of vitamin K as a therapeutic agent, even 500 times the recommended daily allowance for a long period, with the exception of some rare hypersensitivity reactions that may occur when given intravenously (32). According to Penniston and Tanumihardjo (33), vitamin A modulates vitamin D 3 toxicity because of an antagonism between vitamins A and D at the receptor level and an interaction with calcium regulating hormones such as parathyroid hormone (34), whereas the receptors for retinoic acid are located on osteoblasts and osteoclasts (35). Therefore, the therapeutic doses of vitamin A are given safely for a long period to ameliorate the manifestations of hypervitaminosis D 3 , whereas a low incidence of transient toxic effects of vitamin A may be expected and tolerated (36,37).…”

Section: Discussionmentioning

confidence: 99%

Comparison between the protective effects of vitamin K and vitamin A on the modulation of hypervitaminosis D3 short-term toxicity in adult albino rats

Elshama¹,

Osman²,

El-Kenawy³

et al. 2016

Turk J Med Sci

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Background/aim: Vitamin D 3 has increased risk of toxicity due to its common use in multivitamin preparations. Vitamin K and vitamin A play an important role in vitamin D action. The goal of the current study was to compare the protective effects of vitamin K and vitamin A on the modulation of hypervitaminosis D 3 toxicity in rats by assessing serum calcium, renal function tests, cardiac enzymes, and related histopathological changes.Materials and methods: Eighty adult albino rats were divided into four groups; each group consisted of 20 rats. The first group received water; the second received a toxic dose of vitamin D 3 ; the third received a toxic dose of vitamin D 3 with vitamin A; and the fourth received a toxic dose of vitamin D 3 with vitamin K.Results: Vitamin D 3 toxicity led to significant abnormalities of cardiac enzymes, renal function tests, and serum calcium associated with histopathological changes in the kidney, heart, lung, adrenal gland, and aorta. Individual administration of vitamin A or vitamin K with a toxic dose of vitamin D improved the biochemical and histopathological abnormalities of hypervitaminosis D 3 . Conclusion:Vitamins A and K showed the same protective effects in the modulation of hypervitaminosis D 3 short-term toxicity.

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“…Naturally occurring dietary sources of vitamin D include eggs, liver, and fatty fish, but the dominant sources of dietary vitamin D in the United States are fortified dairy products and breakfast cereal. Although many individuals take supplemental vitamin D, most multivitamins also contain retinol, an antagonist of actions of vitamin D on mineral homeostasis and bone function, possibly acting through competition for the retinoid X receptor (19).…”

Section: Introductionmentioning

confidence: 99%

Vitamin D Intake and the Risk for Pancreatic Cancer in Two Cohort Studies

Skinner

Michaud²,

Giovannucci

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

151

105

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Vitamin D and its analogues exhibit potent antitumor effects in many tissues, including the pancreas. Normal and malignant pancreatic tissues were recently shown to express high levels of vitamin D 1-A-hydroxylase, which converts circulating 25-hydroxyvitamin D to active 1,25-dihydroxyvitamin D. We examined associations between dietary intake of vitamin D, calcium, and retinol and subsequent risk for pancreatic cancer. We conducted prospective studies in

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Vitamin A Antagonizes Calcium Response to Vitamin D in Man

Cited by 150 publications

References 39 publications

Inhibition of lung carcinogenesis by 1α,25‐dihydroxyvitamin D₃ and 9‐cis retinoic acid in the A/J mouse model: Evidence of retinoid mitigation of vitamin D toxicity

Inhibition of lung carcinogenesis by 1α,25‐dihydroxyvitamin D₃ and 9‐cis retinoic acid in the A/J mouse model: Evidence of retinoid mitigation of vitamin D toxicity

Comparison between the protective effects of vitamin K and vitamin A on the modulation of hypervitaminosis D3 short-term toxicity in adult albino rats

Vitamin D Intake and the Risk for Pancreatic Cancer in Two Cohort Studies

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Vitamin A Antagonizes Calcium Response to Vitamin D in Man

Cited by 150 publications

References 39 publications

Inhibition of lung carcinogenesis by 1α,25‐dihydroxyvitamin D3 and 9‐cis retinoic acid in the A/J mouse model: Evidence of retinoid mitigation of vitamin D toxicity

Inhibition of lung carcinogenesis by 1α,25‐dihydroxyvitamin D3 and 9‐cis retinoic acid in the A/J mouse model: Evidence of retinoid mitigation of vitamin D toxicity

Comparison between the protective effects of vitamin K and vitamin A on the modulation of hypervitaminosis D3 short-term toxicity in adult albino rats

Vitamin D Intake and the Risk for Pancreatic Cancer in Two Cohort Studies

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Inhibition of lung carcinogenesis by 1α,25‐dihydroxyvitamin D₃ and 9‐cis retinoic acid in the A/J mouse model: Evidence of retinoid mitigation of vitamin D toxicity

Inhibition of lung carcinogenesis by 1α,25‐dihydroxyvitamin D₃ and 9‐cis retinoic acid in the A/J mouse model: Evidence of retinoid mitigation of vitamin D toxicity