Cadmium, iron and zinc interaction and hematological parameters in rat dams and their offspring

Mikolić, Anja; Schönwald, Neala; Piasek, Martina

doi:10.1016/j.jtemb.2016.08.008

Cited by 8 publications

(4 citation statements)

References 42 publications

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“…A decreased platelet count (PLT) and serum total cholesterol were also observed. Cadmium-induced unfavorable changes in blood morphology are well documented in the available literature [21,22,23].…”

Section: Discussionmentioning

confidence: 99%

Alleviating Effect of α-Lipoic Acid and Magnesium on Cadmium-Induced Inflammatory Processes, Oxidative Stress and Bone Metabolism Disorders in Wistar Rats

Markiewicz−Górka

Pawlas

Jaremków

et al. 2019

IJERPH

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Cadmium exposure contributes to internal organ dysfunction and the development of chronic diseases. The aim of the study was to assess the alleviating effect of α-lipoic acid and/or magnesium on cadmium-induced oxidative stress and disorders in bone metabolism, kidney and liver function, and hematological and biochemical parameters changes. Male rats were exposed to cadmium (30 mg Cd/kg of feed) for three months. Some animals exposed to Cd were supplemented with magnesium (150 mg Mg/kg of feed) and/or with α-lipoic acid (100 mg/kg body weight, four times a week). Cd intake inhibited body weight gain and lowered hemoglobin concentration, whereas it increased the activities of liver enzymes, as well as the level of oxidative stress, CTX-1 (C-terminal telopeptide of type I collagen, bone resorption marker), and CRP (C-reactive protein, marker of inflammation); it decreased vitamin D3, GSH (reduced glutathione), and the serum urea nitrogen/creatinine index. Mg and/or α-lipoic acid supplementation increased the antioxidant potential, and partially normalized the studied biochemical parameters. The obtained results show that both magnesium and α-lipoic acid decrease oxidative stress and the level of inflammatory marker, as well as normalize bone metabolism and liver and kidney function. Combined intake of α-lipoic acid and magnesium results in reinforcement of the protective effect; especially, it increases antioxidant defense.

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Section: Discussionmentioning

confidence: 99%

Alleviating Effect of α-Lipoic Acid and Magnesium on Cadmium-Induced Inflammatory Processes, Oxidative Stress and Bone Metabolism Disorders in Wistar Rats

Markiewicz−Górka

Pawlas

Jaremków

et al. 2019

IJERPH

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“…During pregnancy, both inhalational and oral Cd absorption increase [ 35 , 38 , 39 ]. This effect can be explained by the physiological changes that take place during this stage, like increased respiratory rate, decreased gastrointestinal motility and decreased gastric emptying [ 40 ].…”

Section: Cadmium Distribution During Pregnancymentioning

confidence: 99%

“…Also during this stage, Cd exposure has been associated with altered concentrations of micronutrients in internal organs. For instance, iron levels in liver, kidneys, placenta and fetus decrease [ 39 , 44 ]; zinc levels increase in liver and decrease in kidneys and placenta [ 44 , 64 , 92 ], and copper levels show contrasting behaviors in liver and kidneys [ 51 , 64 ]. Although there are differences in the route of Cd administration, all studies conclude that Cd induced lower micronutrient concentrations in the fetuses.…”

Section: Toxic Effects In Damsmentioning

confidence: 99%

Cadmium Handling, Toxicity and Molecular Targets Involved during Pregnancy: Lessons from Experimental Models

Jacobo-Estrada

Santoyo-Sánchez

Thévenod

et al. 2017

IJMS

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Even decades after the discovery of Cadmium (Cd) toxicity, research on this heavy metal is still a hot topic in scientific literature: as we wrote this review, more than 1440 scientific articles had been published and listed by the website during 2017. Cadmium is one of the most common and harmful heavy metals present in our environment. Since pregnancy is a very particular physiological condition that could impact and modify essential pathways involved in the handling of Cd, the prenatal life is a critical stage for exposure to this non-essential element. To give the reader an overview of the possible mechanisms involved in the multiple organ toxic effects in fetuses after the exposure to Cd during pregnancy, we decided to compile some of the most relevant experimental studies performed in experimental models and to summarize the advances in this field such as the Cd distribution and the factors that could alter it (diet, binding-proteins and membrane transporters), the Cd-induced toxicity in dams (preeclampsia, fertility, kidney injury, alteration in essential element homeostasis and bone mineralization), in placenta and in fetus (teratogenicity, central nervous system, liver and kidney).

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“…Among them, the classical theory holds that cadmium can produce oxidative stress and lipid peroxidation by interfering with redox reaction which can induce cell apoptosis [6]. Moreover, cadmium interferes with the steady state of basic metal ions, such as calcium ion signaling [7,8], and interacts with metalloproteins to induce metallothionein expression [9]. In addition, cadmium interacts with nonmetallic proteins such as those containing active cysteine.…”

Section: Introductionmentioning

confidence: 99%

Phospholipase D1 Ameliorates Apoptosis in Chronic Renal Toxicity Caused by Low‐Dose Cadmium Exposure

Deng

Wang

Geng

et al. 2020

BioMed Research International

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Exposure to cadmium (Cd), a common heavy metal used in industry, can result in long-term chronic toxicity. It has been well characterized that kidneys are the main organs that are targeted by toxicity, which can cause apoptosis, necrosis, and atrophy of renal tubular epithelial cells. However, the molecular mechanisms associated with Cd toxicity remain unclear. In this study, the expression of renal proteins in Sprague-Dawley rats exposed to chronic Cd was analyzed with iTRAQ proteomics. Bioinformatics analysis indicated that phospholipase D1 (PLD1) was significantly underexpressed and may correlate strongly with Cd-induced chronic kidney impairment. Previous studies have shown that PLD1 promotes cell proliferation and inhibits apoptosis, indicating that PLD1 may be implicated in the pathogenesis of kidney injury induced by Cd. Studies in vivo and in vitro all demonstrate that the mRNA and protein levels of PLD1 decrease significantly both in kidney tissue and in proximal tubular cell lines exposed to Cd. Overexpression of PLD1 and its downstream product PA could ameliorate Cd-induced apoptosis. Moreover, we identified that miR-122-5p was a regulatory miRNA of PLD1. miR-122-5p was overexpressed after Cd exposure and promoted cell apoptosis by downregulating PLD1 through binding the 3′UTR of the locus at 1761–1784 nt. In conclusion, our results indicated that PLD1 and its downstream PA were strongly implicated in Cd-induced chronic kidney impairment and could be a novel player in the defense against Cd-induced nephrotoxicity.

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Cadmium, iron and zinc interaction and hematological parameters in rat dams and their offspring

Cited by 8 publications

References 42 publications

Alleviating Effect of α-Lipoic Acid and Magnesium on Cadmium-Induced Inflammatory Processes, Oxidative Stress and Bone Metabolism Disorders in Wistar Rats

Alleviating Effect of α-Lipoic Acid and Magnesium on Cadmium-Induced Inflammatory Processes, Oxidative Stress and Bone Metabolism Disorders in Wistar Rats

Cadmium Handling, Toxicity and Molecular Targets Involved during Pregnancy: Lessons from Experimental Models

Phospholipase D1 Ameliorates Apoptosis in Chronic Renal Toxicity Caused by Low‐Dose Cadmium Exposure

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