Gene

Biology

Heat shock protein

Endocrinology

Biochemistry

Zinc

Immunology

Hsp70

Homeostasis

Organic chemistry

Superoxide dismutase

Immune system

Lipid peroxidation

Oxidative stress

Chemistry

Metallothionein

Cadmium

Zebrafish

Chemosphere

In the study, zebrafish were exposed to 0 and 200 μg/L Zn for 8 weeks, and then both groups were transferred to water including 0, 100, and 200 μg/L Cd for 4 days, respectively. Acute Cd exposure caused negative effects on stress defense, immune, and metal transport systems by increasing lipid peroxidation, iNOS activity and mRNA levels of il-6 and inos, and decreasing Cu/Zn-SOD and HSP70 levels, and mRNA levels of sod1, cat, hsp70, p65, mtf-1, znt5, zip7, atp7a, and atp7b. Lipid peroxidation was significantly reduced by Zn pre-exposure under Cd exposure, which may be explained by the enhanced stress defense capacity and the weaken inflammatory response. Firstly, Zn pre-exposure increased MTs and HSP70 levels and CAT activity in Cd-free water, which may facilitate fish quick response to Cd. Secondly, Zn pre-exposure reduced Cd accumulation at 100 and 200 μg/L Cd, down-regulated il-6 and il-1β at 100 μg/L Cd and p65 at 200 μg/L Cd, and increased Cu/Zn-SOD and CAT activities at 200 μg/L Cd. Thirdly, Zn pre-exposure alone up-regulated transcription factors (hsf1, hsf2, and mtf-1, and nrf2) and their target genes (sod1, cat, hsp70, and mt2) under Cd exposure in a dose-dependent manner. It should be noted that Zn pre-exposure down-regulated several metal transport genes dramatically at 0 and 100 μg/L Cd, which may be an important mechanism for reducing Cd import into livers. Overall, long-term and environmental Zn pre-exposure mitigated Cd toxicity by the enhanced stress defense capacity and the down-regulated metal transport and inflammatory responses.

Negative effects of acute cadmium on stress defense, immunity, and metal homeostasis in liver of zebrafish: The protective role of environmental zinc dpre-exposure