Reduced intestinal calcium and dietary calcium intake, increased aluminum absorption, and tissue concentration in the rat

Provan, Spencer D.; Yokel, Robert A.

doi:10.1007/bf02917183

Cited by 21 publications

(3 citation statements)

References 24 publications

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“…Like iron, calcium (Ca) status impacts on aluminium absorption and accumulation. Dietary calcium deficiency increased the absorption of aluminium from aluminium chloride, and the extent of tissue aluminium accumulation, and aluminium-induced neuropathology in rats (Provan & Yokel, 1990;Taneda, 1984). Increased calcium concentrations decreased aluminium uptake from the chloride and its appearance in plasma in studies that used the rat everted gut sac and in situ rat gut technique, suggesting a common uptake mechanism for aluminium, introduced as the chloride, and calcium (Cunat et al, 2000;Feinroth et al, 1982).…”

Section: Calciummentioning

confidence: 99%

Safety of aluminium from dietary intake ‐ Scientific Opinion of the Panel on Food Additives, Flavourings, Processing Aids and Food Contact Materials (AFC)

2008

EFS2

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Following a request from the Commission, the Panel on Food Additives, Flavourings, Processing Aids and Food Contact Materials (AFC) was asked to provide a scientific opinion on the safety of aluminium from all sources of dietary intake. In the event the estimated exposure for a particular sub-group(s) is found to exceed the Provisional Tolerable Weekly Intake, a detailed breakdown by exposure source should be provided. Aluminium occurs naturally in the environment and is also released due to anthropogenic activities such as mining and industrial uses, in the production of aluminium metal and other aluminium compounds. A variety of aluminium compounds are produced and used for different purposes, such as in water treatment, papermaking, fire retardant, fillers, food additives, colours and pharmaceuticals. Aluminium metal, mainly in the form of alloys with other metals, has many uses including in consumer appliances, food packaging and cookware. The major route of exposure to aluminium for the general population is through food. Aluminium in drinking water represents another, minor, source of exposure. Additional exposures may arise from the use of aluminium compounds in pharmaceuticals and consumer products. Most unprocessed foods typically contain less than 5 mg aluminium/kg. Higher concentrations (mean levels 5 to 10 mg/kg) were often found in breads, cakes and pastries (with biscuits having the highest levels), some vegetables (with mushrooms, spinach, radish, swiss card, 1 For citation purposes: Scientific Opinion of the Panel on Food Additives, Flavourings, Processing Aids and Food Contact Materials on a request from European Commission on Safety of aluminium from dietary intake.

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Section: Calciummentioning

confidence: 99%

Safety of aluminium from dietary intake ‐ Scientific Opinion of the Panel on Food Additives, Flavourings, Processing Aids and Food Contact Materials (AFC)

2008

EFS2

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“…In animal studies, calcium deficiency in the diet has been shown to increase the rate and amount of Al absorption. [ 13 14 ] Vitamin D supplementation may increase Al content in the muscles and hearts. Besides, the parathyroid hormone can increase the absorption of Al by situmilating renal synthesis of 1,25-dihydroxyvitamin D3.…”

Section: Introductionmentioning

confidence: 99%

Is aluminum exposure a risk factor for neurological disorders?

İnan-Eroğlu

Ayaz

2018

J Res Med Sci

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Aluminum (Al) is widely found in the nature. Although the relation between Al and neurodegenerative diseases is still controversial, Al is related with many brain diseases including Alzheimer's disease, Parkinson's disease, and multiple sclerosis. Al exposure occurs mainly through environment, occupational, and dietary factors for humans. Al exposure with diet can be through foods, food additives, water, and contamination of Al equipment/utensils. The aim of this review is to summarize various hypotheses, which link Al and neurodegeneration, and to determine the roles of Al exposure through different sources including diet, environment, and occupation. Future studies should be done in vulnerable subgroups of population including children, patients receiving antacid or Al-containing pharmeteucials on a daily basis, patients with reduced renal function, and patients on parenteral nutrition regimens that are likely to be affected by possible adverse health effects of Al. In addition, gender, age, and Al interactions need to be determined. One of the most important challanges in future epidemiological studies is to determine which variables should be controlled. In addition, experimental studies should be more focused and translational. In this context, exposure dose, dose–response effects, and time lapse between exposures and cognitive assessments are very important.

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“…Hence, it is evident from previous results that the decrease in FSH and LH might be related to a deficiency of ionized calcium. Furthermore, Ca 2+ deficiency might lead to aluminum accumulation in different tissues, because Ca 2+ deficiency cause excess parathyroid hormone (PTH) secretion and PTH absorbs aluminum along with Ca 2+ from renal tubules (Provan & Yokel 1990). The current study demonstrates that co-administration of propolis and vitamin E mitigates the toxic effects of AlCl 3 in a timedependent manner, supporting the results of a previous study in which propolis ameliorated the toxic effect of AlCl 3 on renal histology of wistar albino rats (El-Kenawy et al 2014).…”

Section: Discussionmentioning

confidence: 99%

Ethanolic extract of propolis and vitamin E attenuates metal-induced testicular necrosis: time-related study on male reproductive system in albino mice

Sajjad

Saeed

Malik

et al. 2020

The European Zoological Journal

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This study was designed to investigate the protective effects of propolis and vitamin E against time-related metal (aluminum chloride)-induced toxicity on the male reproductive system in albino mice (n = 63). Animals were randomly divided into seven groups (n = 9 each). Group I (control) received 0.9% saline solution; group II was given 50 mg/kg of aluminum chloride (AlCl 3 ); groups III and IV were administered vitamin E (150 mg/kg) and propolis (50 mg/kg), respectively; and groups V, VI and VII were administered AlCl 3 + vitamin E, AlCl 3 + propolis, and AlCl 3 + vitamin E + propolis, respectively, for 45 days. Animals were sacrificed; blood and tissue samples were collected (thrice; fortnightly) for the estimation of hormones i.e., Follicle stimulating hormone (FSH), Luteinizing hormone (LH) and testosterone using Enzyme linked immunosorbent assay (ELISA). Testicular histology, testicular weight, sperm count and motility were estimated. Group II revealed a highly significant decrease in LH, FSH, testosterone, testis weight, sperm count and motility. Groups III-VII showed a significant increase in LH, FSH, testosterone, organ weight, sperm count and motility in the 3 rd sampling, as compared to group II. Hence, it is concluded that vitamin E and propolis, acting individually as well as synergistically, mitigate metal-induced timerelated toxicity on the reproductive system and testicular histology of male mice.

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Reduced intestinal calcium and dietary calcium intake, increased aluminum absorption, and tissue concentration in the rat

Cited by 21 publications

References 24 publications

Safety of aluminium from dietary intake ‐ Scientific Opinion of the Panel on Food Additives, Flavourings, Processing Aids and Food Contact Materials (AFC)

Safety of aluminium from dietary intake ‐ Scientific Opinion of the Panel on Food Additives, Flavourings, Processing Aids and Food Contact Materials (AFC)

Is aluminum exposure a risk factor for neurological disorders?

Ethanolic extract of propolis and vitamin E attenuates metal-induced testicular necrosis: time-related study on male reproductive system in albino mice

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