Pro-inflammatory properties of cadmium.

Abstract

Cadmium is a toxic and carcinogenic heavy metal that nowadays constitutes a serious environmental health problem. The aim of this study is to review the effects of cadmium on selected inflammatory mediators and markers, such as NF-κB and AP-1 transcription factors, IL-6, TNF-α, IL-1β cytokines, IL-8 or MIP-2 chemokine, MPO, iNOS, MMPs and COX-2 enzymes, PGE 2 (product of COX-2 enzyme), ICAM-1, VCAM-1 and PECAM-1 adhesion molecules, and CRP. The research strategy identified articles available in Medline, published between 1998 and 2012; we included both in vivo and in vitro studies carried out on humans and rodents. Most of the reviewed research findings suggest that cadmium in micromolar concentrations (especially in the 1-10 μM range) causes up-regulation of the mediators and markers of inflammation, and appears to have pro-inflammatory properties. However, it is worth mentioning that a contradictory or even opposite hypothesis exists, which suggests cadmium to be an anti-inflammatory factor. Further research including detailed histological analyses should solve this discrepancy. Nevertheless, it appears that the main reason for these contradictory findings is the experimental setup: different biological systems analyzed and different doses of cadmium applied.

The Protective Effects of Melatonin Against Oxidative Stress and Inflammation Induced by Acute Cadmium Exposure in Mice Testis

“…Cd exposure can also induce the production of pro-inflammatory cytokines, such as IL-1β and TNF-α [27], and these two cytokines were also detected in this study as they are mainly produced due to oxidative stress [76][77][78]. IL-1β and TNF-α are characteristically produced by activated macrophages and can trigger apoptosis during inflammation [79,80].…”

“…Melatonin administration ameliorates the proinflammatory state and oxidative stress in diabetic fatty rats [26]. The main mechanisms of the toxic action of Cd in cells include a decrease in anti-oxidant potential and oxidative stress, and secondary injury due to acute Cd exposure is thought to activate a large number of inflammatory and cytotoxic mediators, especially the production of TNF-α and IL-1β [27]. Previous studies showed that Cd could induce oxidation and inflammation in the liver of rats and the testis of mice [28,29].…”

Maternal urinary cadmium concentrations in relation to preterm birth in the Healthy Baby Cohort Study in China

“…PROM primarily arises from inappropriate initiation of an intrauterine inflammatory cascade (Challis et al, 2009). Cd has been shown to stimulate the production of pro-inflammatory cytokines, such as IL-1β and TNF-α (Olszowski et al, 2012). It is interesting to speculate that the observed association between maternal urinary Cd and pPROM may be representing an enhanced maternal response to inflammation via Cd exposure leading to pPROM.…”

Effects of Nano-zinc on Biochemical Parameters in Cadmium-Exposed Rats

“…Cadmium exposure occurs by the ingestion of contaminated food and water, or the inhalation of polluted air [3,4]. The mechanism of cadmium toxicity consists of binding to sulphur (−SH) groups of proteins, enzymes, and glutathione, inhibiting the function of these biomolecules, generating oxidative stress, decreasing anti-oxidant and thiol group status, binding to Ca 2+ binding proteins, inhibiting DNA methylation and DNA repair, and damaging cells and carcinogenicity [5][6][7]. The International Agency of Research on Cancer has classified this metal and its compounds as group 1 human carcinogen [3].…”