Nutrients, Vol. 17, Pages 702: The Preventive Impact of Chokeberry (Aronia melanocarpa L.) Extract Regarding the Disruption of Calcium and Phosphorus Homeostasis and Chosen Pathways of Its Regulation in an Animal Model of General Population Exposure to Cadmium

Nutrients, Vol. 17, Pages 702: The Preventive Impact of Chokeberry (Aronia melanocarpa L.) Extract Regarding the Disruption of Calcium and Phosphorus Homeostasis and Chosen Pathways of Its Regulation in an Animal Model of General Population Exposure to Cadmium

Nutrients doi: 10.3390/nu17040702

Authors:
Małgorzata M. Brzóska
Małgorzata Gałażyn-Sidorczuk
Joanna Rogalska

Background: Our previous research in an experimental model of current environmental human exposure to cadmium (Cd) (female rats fed a diet containing Cd at 1 and 5 mg/kg for up to 2 years) revealed that chronic treatment with this toxic element destroyed the metabolism of the bone tissue, decreased mineralisation, and weakened bone biomechanical properties, whereas the co-administration of a 0.1% chokeberry (Aronia melanocarpa L. (Michx.) Elliott berry) extract (AME) ameliorated the osteotoxic action of Cd. Methods: In this study, it was explored whether the unfavourable effect of Cd and the protective action of AME might be mediated by the impact on the metabolism of bone essential elements such as calcium (Ca) and inorganic phosphorus (Pi), including the pathways of its regulation by calciotropic hormones (parathormone—PTH, calcitonin—CT, and 1,25-dihydroxyvitamin D3—1,25(OH)2D3) and Klotho. Results: Low-level Cd treatment (1 mg/kg) caused only a temporary elevation in the serum PTH concentration and a decline in the concentration of CT. Moderate treatment with Cd (5 mg/kg) destroyed the body homeostasis of both mineral elements (lowered their concentrations in the serum and enhanced urinary loss), influenced the serum concentrations of Klotho and calciotropic hormones, as well as reduced the concentrations of 25-hydroxyvitamin D 1alpha-hydroxylase (1alpha-OHase) and 1,25(OH)2D3 in the kidney. The application of AME during Cd intoxication improved the pathways involved in maintaining Ca and Pi homeostasis and allowed subjects to maintain the proper levels of these elements in the serum and urine. Conclusions: In conclusion, Cd at low-to-moderate exposure may exert an unfavourable impact on bone by influencing the pathways involved in regulating Ca and Pi metabolism and destroying the body status of these minerals. It seems that the possible mechanism of the osteoprotective effect of AME during chronic intoxication with this toxic element involves normalization of the concentrations of calciotropic hormones and Klotho in the serum and improvement of the homeostasis of Ca and Pi. This study provided further evidence that chokeberry products may be an effective strategy in counteracting the unfavourable effects of chronic low-to-moderate exposure to Cd.

​Background: Our previous research in an experimental model of current environmental human exposure to cadmium (Cd) (female rats fed a diet containing Cd at 1 and 5 mg/kg for up to 2 years) revealed that chronic treatment with this toxic element destroyed the metabolism of the bone tissue, decreased mineralisation, and weakened bone biomechanical properties, whereas the co-administration of a 0.1% chokeberry (Aronia melanocarpa L. (Michx.) Elliott berry) extract (AME) ameliorated the osteotoxic action of Cd. Methods: In this study, it was explored whether the unfavourable effect of Cd and the protective action of AME might be mediated by the impact on the metabolism of bone essential elements such as calcium (Ca) and inorganic phosphorus (Pi), including the pathways of its regulation by calciotropic hormones (parathormone—PTH, calcitonin—CT, and 1,25-dihydroxyvitamin D3—1,25(OH)2D3) and Klotho. Results: Low-level Cd treatment (1 mg/kg) caused only a temporary elevation in the serum PTH concentration and a decline in the concentration of CT. Moderate treatment with Cd (5 mg/kg) destroyed the body homeostasis of both mineral elements (lowered their concentrations in the serum and enhanced urinary loss), influenced the serum concentrations of Klotho and calciotropic hormones, as well as reduced the concentrations of 25-hydroxyvitamin D 1alpha-hydroxylase (1alpha-OHase) and 1,25(OH)2D3 in the kidney. The application of AME during Cd intoxication improved the pathways involved in maintaining Ca and Pi homeostasis and allowed subjects to maintain the proper levels of these elements in the serum and urine. Conclusions: In conclusion, Cd at low-to-moderate exposure may exert an unfavourable impact on bone by influencing the pathways involved in regulating Ca and Pi metabolism and destroying the body status of these minerals. It seems that the possible mechanism of the osteoprotective effect of AME during chronic intoxication with this toxic element involves normalization of the concentrations of calciotropic hormones and Klotho in the serum and improvement of the homeostasis of Ca and Pi. This study provided further evidence that chokeberry products may be an effective strategy in counteracting the unfavourable effects of chronic low-to-moderate exposure to Cd. Read More

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