Protective Effect of Aronia Melanocarpa Polyphenols on Cadmium Accumulation in the Body: A Study in a Rat Model of Human Exposure to this Metal

Abstract

Recently a growing attention has been paid to the possibility of using biologically active compounds, including polyphenols, for the prevention of unfavourable effects of exposure to xenobiotics. The study was aimed to investigate, in a female rat model, whether consumption of Aronia melanocarpa polyphenols (AMP) under chronic exposure to cadmium (Cd) decreases the gastrointestinal absorption and body burden of this heavy metal. For this purpose, Cd turnover (apparent absorption, retention in the body, concentration in the blood, soft tissues and bone tissue, total pool in internal organs, faecal and urinary excretion) was evaluated in the female Wistar rats who were administered only a 0.1% aqueous extract of AMP (prepared from the powdered extract containing 65.74% of polyphenols) as drinking fluid or/and Cd in diet (1 and 5 mg/kg) for up to 24 months. AMP administration under the low Cd treatment (1 mg/kg diet) had only a very slight protective impact against this metal accumulation in the organism, whereas polyphenols application under moderate exposure (5 mg Cd/kg diet) significantly decreased apparent absorption and retention in the body, and increased urinary concentration of this xenobiotic, resulting in its lower concentration in the blood and lower accumulation in soft tissues (mainly in the liver and kidneys) and bone tissue. Based on the study, it can be concluded that consumption of polyphenol- rich products may prevent Cd absorption from the diet polluted by this metal and its accumulation in the females' body, and thus also prevent its toxic action.

The Mechanism of the Osteoprotective Action of a Polyphenol-Rich Aronia melanocarpa Extract during Chronic Exposure to Cadmium is Mediated by the Oxidative Defense System

“…Data provided by Kowalczyk et al [15] and our recent findings [6,22,23] seem to indicate that the consumption of chokeberries and their products may prevent Cd accumulation in the body and its toxic action. Using a female rat model of low and moderate lifetime human exposure to Cd (1 and 5 mg Cd/kg diets, respectively, for up to 24 months), we have revealed that a polyphenol-rich AME may decrease the gastrointestinal absorption and body burden of this xenobiotic (including its accumulation in the liver, kidneys, and bone tissue) [22], as well as significantly prevent disturbances induced by this heavy metal in the bone turnover, and changes in the bone mineral status [23]. Taking into account the pro-oxidative action of Cd and oxidative stress involvement in the mechanisms of this metalʼs toxicity, including osteotoxic action [3,5,[24][25][26][27][28], and the strong antioxidative properties of chokeberry [13,14,[18][19][20], we have hypothesized that the osteoprotective effect reported by us [23] of AME during chronic exposure to Cd may be mediated by the oxidative defense system (the system of defense from oxidative processes and oxidative stress).…”

“…Nowadays, the consumption of aronia berries is widely recommended as one of the most abundant sources of compounds having a beneficial influence on the organism, and the richest source among plant materials of anthocyanins, which are characterized by strong antioxidative properties [13,14,[18][19][20][21]. Data provided by Kowalczyk et al [15] and our recent findings [6,22,23] seem to indicate that the consumption of chokeberries and their products may prevent Cd accumulation in the body and its toxic action. Using a female rat model of low and moderate lifetime human exposure to Cd (1 and 5 mg Cd/kg diets, respectively, for up to 24 months), we have revealed that a polyphenol-rich AME may decrease the gastrointestinal absorption and body burden of this xenobiotic (including its accumulation in the liver, kidneys, and bone tissue) [22], as well as significantly prevent disturbances induced by this heavy metal in the bone turnover, and changes in the bone mineral status [23].…”

“…Zinc not only stimulates osteoblasts proliferation and differentiation, but it also suppresses osteoclasts differentiation by, among others, antagonizing NF-κB activation [27,33,34]. Polyphenols, due to their ability to bind Cd 2+ [4], may decrease the body burden of Cd and thus protect against the effects of its direct and indirect action, resulting in the improvement of the oxidative/antioxidative balance and bone turnover [6,15,22,23]. It is also necessary to take into consideration that the molecular mechanisms of the beneficial impact of polyphenols on bone tissue metabolism might be related to the ability of these compounds to enhance the production of nitric oxide, which is essential for the induction of new bone formation [35], as well as to induce the nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidant gene expressions and thereby to decrease the oxidative status [7].…”

“…We have previously reported that AME administration under exposure to the 1 mg Cd/kg diet had only a very slight protective impact against this metalʼs accumulation in the organism, whereas its application under treatment with the 5 mg Cd/kg diet significantly decreased the apparent absorption and retention in the body and increased urinary concentration of this heavy metal, resulting in its lower concentration in the blood and lower accumulation in soft tissues (mainly in the liver and kidneys) and bone tissue. Due to the lower Cd transportation into the sites of its toxic action, including bone tissue, and faster elimination from the organism of the absorbed metal, the amounts of Cd at the sites of its action, including oxidative action, were lower, and thus the effects of its toxicity were less intensified or even completely counteracted by AME administration [22]. Since Cd, even at low concentrations, may directly influence bone tissue cell activity and oxidative/antoxidative balance, it seems reasonable to assume that the beneficial impact of AME on the oxidative/antioxidative status of the bone tissue under the higher of the investigated levels of Cd treatment was, at least to some extent, the result of the lower bone concentration of this metal.…”

“…The aim of the present paper was to investigate this hypothesis. For this purpose, numerous indices of the oxidative/antioxidative bone status and markers of oxidative protein, lipid, and DNA damage were determined in the bone tissue, and mutual dependences between these parameters, indices of bone turnover (Table 1S, Supporting Information), and bone mineral status (Table 2S, Supporting Information) previously determined in these animals [23] as well as Cd concentration in the bone tissue (Table 3S, Supporting Information) [22] were evaluated.…”