Body burden of cadmium in man at low level of exposure

Salmela, S.; Vuori, Erkki; Huunan-Seppälä, A; Kilpiö, Jukka; Sumuvuori, H.

doi:10.1016/0048-9697(83)90126-2

Cited by 14 publications

(6 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Together, the kidneys and liver (Jarup and Akesson 2009) contain ~ 85% of the cadmium body burden, and more than 60% is found in the kidneys in the age range of 30-60 years (Jarup and Akesson 2009;Salmela et al 1983). The accumulation of cadmium in kidneys and liver occurs because intracellular cadmium upregulates detoxifying molecules, such as metallothionein (MT) (Freisinger and Vasak 2013), which sequester the metal ion and thereby counteract its toxic effects.…”

Section: Introductionmentioning

confidence: 99%

Cell organelles as targets of mammalian cadmium toxicity

Lee

Thévenod

2020

Arch Toxicol

View full text Add to dashboard Cite

Ever increasing environmental presence of cadmium as a consequence of industrial activities is considered a health hazard and is closely linked to deteriorating global health status. General animal and human cadmium exposure ranges from ingestion of foodstuffs sourced from heavily polluted hotspots and cigarette smoke to widespread contamination of air and water, including cadmium-containing microplastics found in household water. Cadmium is promiscuous in its effects and exerts numerous cellular perturbations based on direct interactions with macromolecules and its capacity to mimic or displace essential physiological ions, such as iron and zinc. Cell organelles use lipid membranes to form complex tightly-regulated, compartmentalized networks with specialized functions, which are fundamental to life. Interorganellar communication is crucial for orchestrating correct cell behavior, such as adaptive stress responses, and can be mediated by the release of signaling molecules, exchange of organelle contents, mechanical force generated through organelle shape changes or direct membrane contact sites. In this review, cadmium effects on organellar structure and function will be critically discussed with particular consideration to disruption of organelle physiology in vertebrates.

show abstract

Section: Introductionmentioning

confidence: 99%

Cell organelles as targets of mammalian cadmium toxicity

Lee

Thévenod

2020

Arch Toxicol

View full text Add to dashboard Cite

show abstract

“…The kidneys contain ∼60% of the Cd body burden in the age range of 30–60 years ( Salmela et al, 1983 ; Jarup and Akesson, 2009 ). Cd accumulates in the kidneys, in particular the PT, because intracellular Cd induces the upregulation of the protein MT, rich in sulfhydryl (SH) groups that bind the metal ion with high affinity and thereby prevent its toxic effects ( Freisinger and Vasak, 2013 ).…”

Section: Toxicity and The Kidneymentioning

confidence: 99%

Iron and Cadmium Entry Into Renal Mitochondria: Physiological and Toxicological Implications

Thévenod

Lee

Garrick

2020

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Regulation of body fluid homeostasis is a major renal function, occurring largely through epithelial solute transport in various nephron segments driven by Na + /K + -ATPase activity. Energy demands are greatest in the proximal tubule and thick ascending limb where mitochondrial ATP production occurs through oxidative phosphorylation. Mitochondria contain 20–80% of the cell’s iron, copper, and manganese that are imported for their redox properties, primarily for electron transport. Redox reactions, however, also lead to reactive, toxic compounds, hence careful control of redox-active metal import into mitochondria is necessary. Current dogma claims the outer mitochondrial membrane (OMM) is freely permeable to metal ions, while the inner mitochondrial membrane (IMM) is selectively permeable. Yet we recently showed iron and manganese import at the OMM involves divalent metal transporter 1 (DMT1), an H + -coupled metal ion transporter. Thus, iron import is not only regulated by IMM mitoferrins, but also depends on the OMM to intermembrane space H + gradient. We discuss how these mitochondrial transport processes contribute to renal injury in systemic (e.g., hemochromatosis) and local (e.g., hemoglobinuria) iron overload. Furthermore, the environmental toxicant cadmium selectively damages kidney mitochondria by “ionic mimicry” utilizing iron and calcium transporters, such as OMM DMT1 or IMM calcium uniporter, and by disrupting the electron transport chain. Consequently, unraveling mitochondrial metal ion transport may help develop new strategies to prevent kidney injury induced by metals.

show abstract

“…Previous studies already suggested that muscle may form an important Cd pool. 3,4 However, the relevance of these pools in the genesis and progression of Cd-dependent diseases and age-related processes is still unclear.…”

Section: Relative CD Distribution In the Human Bodymentioning

confidence: 99%

“…A limited number of studies have assessed the total human body burden of Cd. Pioneering work in this field stems from studies published from the late 1950ies, [1][2][3][4] and an excellent overview was given by Kjellström in 1979. 5 Total body burden and Cd turnover was previously estimated in subjects being chronically exposed to Cd for a long term or experienced acute intoxication.…”

Section: Introductionmentioning

confidence: 99%

“…6 Relevant studies were performed on bodies of persons who died from sudden or accidental deaths. [3][4][5] An important summary on Cd concentrations in organs and tissues by country was provided by Elinder in 1985. 7 Saltzman et al investigated Cd (as well as Cu, Zn, and Pb) in 26 human cadavers and significantly extended the number of tissues studied to 29.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation