Chronic cadmium exposure induced hepatic cellular stress and inflammation in aged female mice

Abstract

Previous studies have revealed that acute cadmium (Cd) exposure led to inflammation in different organs through an oxidative stress mechanism. However, whether chronic Cd exposure induces inflammation in liver and the mechanistic link between inflammation and cell stress remains unclear. In the present study, we investigated the effects of chronic Cd exposure on hepatic cellular stress and inflammatory responses. Female CD1 mice were administrated with CdCl2 (10 and 100 mg/L) in drinking water for 57 weeks. Our results showed that the mRNA levels of Inos and the protein content of HO‐1, markers of oxidative stress, were markedly increased in Cd‐treated mice. In addition, the protein level of GRP78, the chaperone of endoplasmic reticulum (ER) stress, was significantly increased in Cd‐treated mice. The expression of the proteins CHOP and peIF2α, two proteins downstream of ER stress, was also upregulated in the Cd‐100 mg/L and Cd‐10 mg/L group, respectively. Moreover, there were increased inflammatory cells existing in liver after Cd administration. Besides, there was a significant elevation in the mRNA level of Mip‐2, Il‐10 and Il‐12 in the Cd‐100 mg/L group. The mRNA level of Tgf‐β was also upregulated in Cd‐treated mice. Moreover, we also found that the number of Ki67‐positive hepatic cells was increased in the Cd‐10 mg/L group. Hence, our results indicated that chronic Cd exposure induced oxidative stress, ER stress, inflammatory responses and proliferation in the liver of aged female mice.

Hyperglycemia exacerbates cadmium-induced glomerular nephrosis

“…Cadmium (Cd) is an environmentally abundant toxic heavy metal (Abarikwu et al, 2018;Fan et al, 2018;Zhang et al, 2018). Food and cigarettes are two major sources of human exposure to Cd (Mannino et al, 2004;Ivanova et al, 2017); however, higher levels of exposure to Cd may be seen in occupational settings, such as nickel-cadmium battery manufacturing enterprises.…”

Exploration of the optimal strategy for dietary calcium intervention against the toxicity of liver and kidney induced by cadmium in mice: An in vivo diet intervention study

“…It is partly because there is a large number of metallothionein in these organs, which is easy to bind with heavy metals such as Cd [27]. The toxicity to liver and/or kidneys of mice induced by Cd has been reported in previous studies, which is specifically manifested in liver and kidney dysfunction, oxidative stress and pathological changes [28][29][30][31]. Ca is known as an essential element that is of significance in whole-body growth [32].…”

Mitochondrial GPX4 acetylation is involved in cadmium-induced renal cell ferroptosis

“…Cd is highly toxic and non-biodegradable and has a half-life of 10–30 years [ 11 ]. Numerous studies have indicated that environmental Cd exposure causes damage of multiple organs, including testicles, liver, kidney, bones and lungs [ [12] , [13] , [14] , [15] , [16] ]. Indeed, kidney is a major accumulation organ of Cd, and former studies have shown that chronic exposure to cadmium can trigger renal dysfunction [ 17 , 18 ].…”