Hypervitaminosis A: A Review*

Clark, Leigh

doi:10.1111/j.1751-0813.1971.tb02061.x

Cited by 29 publications

(24 citation statements)

References 37 publications

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“…To elucidate this mechanism further study will be needed. It has been shown that excessive intake of vitamin A leads to a distinct hypervitaminotic, toxic manifestation and this toxic effects of vitamin A seem to be caused by the activation of proteolytic enzymes (Bangham et al 1964;Roels et al 1969;Clark 1971). However, these toxic effects of vitamin A were not seen when retinol was a form bound to the RBP (Dingle et al 1972).…”

Section: Discussionmentioning

confidence: 99%

Vitamin A transport in plasma of diabetic patients.

Wako

Suzuki

Gotō

et al. 1986

Tohoku J. Exp. Med.

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The effects of diabetes on the vitamin A metabolism were studied. The concentrations of plasma retinol and retinyl ester were measured in diabetic patients using high-performance liquid chromatography (HPLC). In diabetic patients, the mean level of retinyl ester was significantly elevated compared to that of normal subjects (diabetes, 68.3+42.5 IU/100 ml of plasma ; study I, 87.6+64.3 IU/100 ml of plasma ; study II vs. normal, 29.8+ 10.3 IU/100 ml of plasma). The ultracentrifugal and column chromatographic studies were carried out to examine the distribution of retinyl ester in patient's plasma. Ultracentrifugation study showed that the mean of 72.6° of retinyl ester was recovered in the lipoproteins of density higher than 1.006 and the remainder was recovered in the chylomicron (d < 1.006). Gel filtration profiles for the separation of plasma vitamin A demonstrated that retinyl ester presented in the HDL, LDL and larger molecular size lipoprotein (suspected to be VLDL) as well as in the chylomicron. vitamin A ; diabetes ; plasma lipoprotein

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Section: Discussionmentioning

confidence: 99%

Vitamin A transport in plasma of diabetic patients.

Wako

Suzuki

Gotō

et al. 1986

Tohoku J. Exp. Med.

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“…The gross bone lesions observed in chronic vitamin A toxicosis include a decreased length and shaft width, metaphyseal flaring, cartilaginous degeneration, exostosis, osteopenia, and fractures (1)(2)(3)(4). Histological data are conflicting; although rickets has been reported in turkey poults (6), osteoporosis with varying degrees of osteoblastic and osteoclastic activity has been documented in most other species (1)(2)(3)(4)(5).…”

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confidence: 95%

“…The nature and extent of these alterations are, however, poorly defined and appear to depend, at least in part, on the animal species tested as well as the dose, duration, and vitamin A preparation used (3)(4)(5)(6). The gross bone lesions observed in chronic vitamin A toxicosis include a decreased length and shaft width, metaphyseal flaring, cartilaginous degeneration, exostosis, osteopenia, and fractures (1)(2)(3)(4). Histological data are conflicting; although rickets has been reported in turkey poults (6), osteoporosis with varying degrees of osteoblastic and osteoclastic activity has been documented in most other species (1)(2)(3)(4)(5).…”

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confidence: 99%

“…We conclude that vitamin A toxicity in rats causes bone lesions, the genesis of which can be explained, at least in part, by a direct effect of the vitamin on skeletal tissue. (Endocrinology 122: [2933][2934][2935][2936][2937][2938][2939]1988) V ITAMIN A toxicity is known to result in alterations of bone and mineral metabolism (1)(2)(3)(4)(5)(6)(7)(8)(9). The nature and extent of these alterations are, however, poorly defined and appear to depend, at least in part, on the animal species tested as well as the dose, duration, and vitamin A preparation used (3)(4)(5)(6).…”

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Effects of Hypervitaminosis A on the Bone and Mineral Metabolism of the Rat*

et al. 1988

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Vitamin A toxicity has been associated with alterations in mineral metabolism and may result in osteopenia, fractures, deformities, and growth arrest. The pathogenesis of the bone lesions that occur in vitamin A toxicity is, however, ill defined and was examined in the present study. The administration of pharmacological doses of vitamin A to growing male rats resulted in weakness and spontaneous fractures. Undecalcified bone histology of vitamin A toxic animals was characterized by increased bone resorption, osteoclastosis, a paucity of trabecular surfaces covered with osteoid, and lesions which appear to be pathognomonic of hypervitaminosis A. The serum calcium and magnesium levels of vitamin A-toxic animals were unremarkable, but serum phosphate levels were significantly higher than control values. Urinary hydroxyproline excretion reflected bone histology and was significantly increased in experimental rats. Circulating levels of the potent bone resorbers, PTH, 1,25-dihydroxyvitamin D, and 25-hydroxyvitamin D, were, however, comparable in vitamin A-toxic and control animals, suggesting a possible direct effect of vitamin A on bone. Subsequently, the effects of vitamin A (retinol) on in vitro collagen synthesis (incorporation of [3H]proline into collagen) and bone resorption (45Ca release from bone) were examined using a fetal rat calvarial culture. Retinol added to the culture medium for 20-24 h in concentrations ranging from 0.5-10 micrograms/ml selectively inhibited collagen synthesis in a dose-dependent fashion. Higher concentrations of retinol were toxic and resulted in a general inhibition of protein synthesis. Bone resorption was stimulated by 0.5 and 2.5 micrograms/ml retinol. We conclude that vitamin A toxicity in rats causes bone lesions, the genesis of which can be explained, at least in part, by a direct effect of the vitamin on skeletal tissue.

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“…Hypervitaminosis A causes vertebral abnormalities and may be compounded by protein-energy malnutrition. 5 ''Crooked calves'' are caused by ingestion of certain Lupinus sp. containing toxic concentrations of the quinolizidine alkaloid, anagyrine, by the Vet Pathol 44: 342-354 (2007) dam, particularly between 40 and 70 days of gestation.…”

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confidence: 99%

Chondrodysplastic Calves in Northeast Victoria

McLaren¹,

Cave²,

Parker³

et al. 2007

Vet Pathol

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Abstract. Outbreaks of chondrodysplasia in calves occur sporadically every 10-15 years, particularly following prolonged drought conditions, throughout Northeastern Victoria and the Southern Table-lands of New South Wales, Australia. An outbreak spanning 2 calving seasons (2003)(2004) involving numerous losses through stillbirth, perinatal loss, and poor growth was investigated. Investigations of 4 representative cases are presented here with a definition of the gross and histopathologic defects and an overview of epidemiologic data gathered from affected farms. Calves showed variable disproportionate dwarfism without arthrogryposis. Long bones were shortened and showed axial rotation. Articular surfaces were distorted with misshapen weight-bearing surfaces associated with variable thickness of articular cartilage. Physes were distorted and variable in thickness with occasional foci of complete closure. The major histologic abnormality in the physes was disorderly development of the zones of cartilage hypertrophy, with reduced number and irregular arrangement of hypertrophic chondrocytes; similar less severe changes were present in the zones of cartilage proliferation. Histochemical staining of the cartilage matrix was variable in intensity, and there was evidence of abnormal resorption of cartilage matrix at the level of the primary spongiosa. Osteoid formation and subsequent bone remodelling seemed unaffected, and diaphyseal cortical bone appeared normal at the gross and light microscopic level. No infectious agents were identified, and other known causes for chondrodysplasia in calves were excluded. The most likely cause for the syndrome was considered to be congenital manganese deficiency. Further surveys of tissue and blood manganese levels from cows and calves with and without clinical signs from the region are planned.

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Hypervitaminosis A: A Review*

Cited by 29 publications

References 37 publications

Vitamin A transport in plasma of diabetic patients.

Vitamin A transport in plasma of diabetic patients.

Effects of Hypervitaminosis A on the Bone and Mineral Metabolism of the Rat*

Chondrodysplastic Calves in Northeast Victoria

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