Cadmium-Induced Pathologies: Where Is the Oxidative Balance

Overview

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Key numbers

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ISSN 1422-0067
Centre for Environmental Sciences, Hasselt University, Agoralaan Building D, Diepenbeek 3590,
Organization (1). Agricultural and industrial activities have led to the entry of Cd into the soil and
feed production (2). This high soil-to-plant transfer rate makes the diet, in general, the primary source
of Cd exposure in humans (3). Vegetables and cereals are the main source of dietary Cd. A lesser
percentage of Cd is found in meat products (4) and fish, except for crustaceans and molluscs that
accumulate large amounts from contaminated aquatic environments (4). Other sources of Cd exposure
include smoking, occupational exposure and house dust (5). Exposure to Cd via house dust is, besides
the food, a significant entry route in areas with Cd-contaminated soils (4). Cadmium is a major
to high leaf Cd concentrations independent of the soil-Cd content (6). In general, the Cd content in
tobacco leaves ranges between 1 and 2 μg/g dry weight resulting in 0.5–1 μg Cd/cigarette.
into the systemic blood circulation of smokers (6). This gives smokers 4–5 times higher Cd levels in
blood and 2–3 times greater amounts of Cd in their kidneys than non-smokers (6). Occupational
burden. Cadmium has a long biological half-time of 10–30 years in the human kidney, with women
iron (Fe) stores (7). Individual variations in Cd sensitivity and kidney Cd accumulation found in
Cd in their kidneys, despite the modest population mean values for Cd body burden (4). Cadmium
nephrotoxicity ensues at renal concentrations of 50 µg Cd/g wet tissue weight (4,7). Although
estimated dietary Cd intake varies widely in different countries (6), daily levels of Cd intake should be
The most important target organ for chronic low-level exposure to Cd is the kidney (8) and is
reflected in proteinuria, calciuria, aminoaciduria, glycosuria and tubular necrosis (6). Chronic low
it also affects bone structure thereby leading to osteoporosis (6). Chronic high levels of Cd exposure
effluents located in the upper reaches of the Jinzu River basin (9). The Itai-Itai disease is clinically
osteoporosis and osteomalacia (9). Furthermore, Cd is also associated with airway inflammation (10),
cardiovascular diseases (11), diabetes (12), neurological diseases (13) and several different organ
level (15). Therefore, the current review focuses on the central role for oxidative stress as an underlying
1. Cellular Mechanisms of Cd Toxicity: A Central Role for Oxidative Stress
essential elements contributes to the cellular uptake mechanisms of Cd (16,17). It is hypothesized that
systems (18–20). Once taken up enterally, Cd reaches the liver where it binds to metallothioneins
(MTs), glutathione (GSH) and other proteins or peptides (21). Metallothioneins induced upon Cd
scavenge reactive oxygen species (ROS) that are produced as a result of Cd-induced oxidative stress (22).
binding stability (15,23). Intracellular Cd, in bound or unbound form, culminates in mitochondrial
damage, and/or cell death (21). Cadmium interferes with mitochondrial oxidative phosphorylation and
in higher doses can inhibit basal respiration (24). It also affects the regulation of mitochondrial genes
such as Hsp60 that play a role in cell protection and programmed cell death (24). Different modes of
death as well as autophagy exhibited by different cell types (25). In brief, it seems that sub-micromolar
concentrations of Cd lead to proliferation or delayed apoptosis, intermediate concentrations of 10 µM
Cd cause various types of apoptotic cell death, and very high concentrations (>50 µM Cd) lead to
necrosis (25).
the cellular redox status plays a crucial role (15,26). An overview on how Cd can disturb the redox
balance is presented in Figure 1 and reviewed in Cuypers et al. (15). In addition, it was demonstrated
As a non-fenton metal, Cd is unable to directly induce ROS (15). However, indirectly, Cd induces
oxidative stress by (1) a displacement of redox-active metals, (2) depletion of redox scavengers, (3)

Methods (brief)

1. Thevenod, F.; Friedmann, J.M. Cadmium-mediated oxidative stress in kidney proximal tubule
1. Thevenod, F.; Friedmann, J.M.; Katsen, A.D.; Hauser, I.A. Up-regulation of multidrug resistance
1. Liu, J.; Kadiiska, M.B.; Corton, J.C.; Qu, W.; Waalkes, M.P.; Mason, R.P.; Liu, Y.; Klaassen, C.D.
1. Wong, K.L.; Klaassen, C.D. Neurotoxic effects of cadmium in young-rats. Toxicol. Appl. Pharm.
chromatography-inductively coupled plasma mass spectrometry. Anal. Chim. Acta 2009, 631,

Implications

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Update history

The five most recent substantive edits to this page, classified major (evidence or structure moved), correction (a published value or statement was wrong and has been fixed), or minor (narrative rewritten without changing the underlying evidence). Each description is derived from what the edit did to this page; the linked commit is the authoritative record, routine regeneration passes are excluded, and the full version history lives in git. When DOI minting comes online (see schema docs), each entry below will also link to a version-pinned DataCite DOI.

Commit	Date	Change	Description
3171d06	2026-08-02	major	1 section added
bc84bfc	2026-08-02	major	6 sections added; narrative text revised