Effect of aluminium on duodenal calcium transport in pregnant and lactating rats treated with bromocriptine

Orihuela, Daniel

doi:10.1016/j.jinorgbio.2007.06.009

Cited by 3 publications

(4 citation statements)

References 29 publications

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“…In addition, osteoblast mineralization in vitro was inhibited by Al-induced decline in transforming growth factor (TGF)-β1 expression and action, and upregulation of Smad7 expression along with decreased protein expressions of osteopontin, osteocalcin and osteosialoprotein (Song et al, 2017). The mineralization of bone is impaired by decreased calcium absorption (Orihuela, 2007), because Al inhibits the synthesis of calbindin, a calcium-binding protein involved in transcellular transport of calcium in enterocytes and inhibits the stimulation of synthesis of osteocalcin (the bone matrix protein) in osteoblasts by vitamin D via cellular unresponsiveness (Fanti et al, 1992;Jeffery et al, 1996;Cox and Dunn, 2001). The expression of cartilage stimulating growth factors, TGF-β1 and BMP-2, were inhibited by Al, thereby suppressing cartilage growth and disrupting cartilage structure .…”

Section: Toxic Action or Effect Selected Referencesmentioning

confidence: 99%

Aluminium toxicosis: a review of toxic actions and effects

Igbokwe

Igwenagu

Igbokwe

2019

Interdisciplinary Toxicology

257

149

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Aluminium (Al) is frequently accessible to animal and human populations to the extent that intoxications may occur. Intake of Al is by inhalation of aerosols or particles, ingestion of food, water and medicaments, skin contact, vaccination, dialysis and infusions. Toxic actions of Al induce oxidative stress, immunologic alterations, genotoxicity, pro-inflammatory effect, peptide denaturation or transformation, enzymatic dysfunction, metabolic derangement, amyloidogenesis, membrane perturbation, iron dyshomeostasis, apoptosis, necrosis and dysplasia. The pathological conditions associated with Al toxicosis are desquamative interstitial pneumonia, pulmonary alveolar proteinosis, granulomas, granulomatosis and fibrosis, toxic myocarditis, thrombosis and ischemic stroke, granulomatous enteritis, Crohn’s disease, inflammatory bowel diseases, anemia, Alzheimer’s disease, dementia, sclerosis, autism, macrophagic myofasciitis, osteomalacia, oligospermia and infertility, hepatorenal disease, breast cancer and cyst, pancreatitis, pancreatic necrosis and diabetes mellitus. The review provides a broad overview of Al toxicosis as a background for sustained investigations of the toxicology of Al compounds of public health importance.

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Section: Toxic Action or Effect Selected Referencesmentioning

confidence: 99%

Aluminium toxicosis: a review of toxic actions and effects

Igbokwe

Igwenagu

Igbokwe

2019

Interdisciplinary Toxicology

257

149

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“…Apparently, the inhibitory effect of Al varies according to thyroid hormone status ( 136 ) . In late pregnancy and mainly during the middle lactation of rats, Al has also been shown to reduce transcellular Ca absorption in the duodenum by interfering with the mechanisms of Ca transport partially mediated by a high serum level of oestrogen and prolactin ( 137 ) .…”

Section: Nutritional Factors Affecting Intestinal Calcium Absorptionmentioning

confidence: 99%

Dietary and pharmacological compounds altering intestinal calcium absorption in humans and animals

et al. 2015

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The intestine is the only gate for the entry of Ca to the body in humans and mammals. The entrance of Ca occurs via paracellular and intracellular pathways. All steps of the latter pathway are regulated by calcitriol and by other hormones. Dietary and pharmacological compounds also modulate the intestinal Ca absorption process. Among them, dietary Ca and P are known to alter the lipid and protein composition of the brush-border and basolateral membranes and, consequently, Ca transport. Ca intakes are below the requirements recommended by health professionals in most countries, triggering important health problems. Chronic low Ca intake has been related to illness conditions such as osteoporosis, hypertension, renal lithiasis and incidences of human cancer. Carbohydrates, mainly lactose, and prebiotics have been described as positive modulators of intestinal Ca absorption. Apparently, high meat proteins increase intestinal Ca absorption while the effect of dietary lipids remains unclear. Pharmacological compounds such as menadione, dl-butionine-S,R-sulfoximine and ursodeoxycholic acid also modify intestinal Ca absorption as a consequence of altering the redox state of the epithelial cells. The paracellular pathway of intestinal Ca absorption is poorly known and is under present study in some laboratories. Another field that needs to be explored more intensively is the influence of the gene × diet interaction on intestinal Ca absorption. Health professionals should be aware of this knowledge in order to develop nutritional or medical strategies to stimulate the efficiency of intestinal Ca absorption and to prevent diseases.

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“…It has been postulated that Al would be able to block the stimulative effect of calmodulin (CaM) on the plasma membrane Ca pump [23], while thyroid hormones would activate the Na/Ca exchanger in enterocytes, possibly via cAMP-mediated pathway [15].…”

Section: Discussionmentioning

confidence: 99%

“…Mucosa-to-serosa Ca flux (JCa ms ) was determined in vitro by an everted duodenal sac technique as previously described in full detail [23]. In short, rats were anesthetized with sodium pentobarbital (50 mg/kg b.w, i.p), proximal segments of small intestine were removed, excised and everted.…”

Section: Measurement Of Ca Absorptionmentioning

confidence: 99%

Effect of aluminium on duodenal calcium transport in pregnant and lactating rats treated with bromocriptine

Cited by 3 publications

References 29 publications

Aluminium toxicosis: a review of toxic actions and effects

Aluminium toxicosis: a review of toxic actions and effects

Dietary and pharmacological compounds altering intestinal calcium absorption in humans and animals

Inhibitory effect of aluminium on calcium absorption in small intestine of rats with different thyroid hormone status

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