ArticleEnvironmental science and pollution research international2020
Inflammatory injury and mitophagy induced by Cr(VI) in chicken liver.
Article in Environmental science and pollution research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 22 citations in OpenAlex.
- Lycopene Attenuates Hexavalent Chromium-Induced Hepatotoxicity in Mice by Modulating the Nrf2 Signaling Pathway and the Unfolded Protein Response.Biological trace element research · 2026Article
- Impact of Vitamin E, Selenium, and Deferasirox on the Negative Effects of Experimental Coccidiosis.Biological trace element research · 2026Article
- Mechanism of Liver Injury Induced by CrAnimals : an open access journal from MDPI · 2026Article
- Hexavalent Chromium Causes Apoptosis and Autophagy by Inducing Mitochondrial Dysfunction and Oxidative Stress in Broiler Cardiomyocytes.Biological trace element research · 2022Article
- Nano-selenium alleviating the lipid metabolism disorder of LMH cells induced by potassium dichromate via down-regulating ACACA and FASN.Environmental science and pollution research international · 2021Article
- Inflammatory injury and mitophagy of the brain in chicken exposed to Cr(VI).Environmental science and pollution research international · 2021Article
- Changes of lipid and bone metabolism in broilers with spontaneous femoral head necrosis.Poultry science · 2021Article
- Effects of embryonic exposure to chromium (VI) on blood parameters and liver microstructure of 1-day-old chickens.Poultry science · 2021Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cr(VI) is a widely used chemical. Excessive Cr(VI) exposure not only causes inflammatory damage but also induces mitophagy. This study aimed to demonstrate the effect of Cr(VI) on inflammatory injury and mitophagy in chicken liver. A total of 120 Hyland Brown cockerels (1 day old) were randomly divided into four groups and orally treated with different Cr(VI) doses (10% median lethal dose, 6% median lethal dose, 2% median lethal dose, and 0% median lethal dose) daily for 45 days to explore the underlying mechanism. Results showed that excessive Cr(VI) increased tumor necrosis factor-α, interleukin-6, and heat shock protein but decreased interferon-γ expression and adenosine triphosphate content in chicken liver. Cr(VI) significantly increased reactive oxygen species production, induced mitochondrial membrane potential collapse, and promoted autophagosome formation. Cr(VI) treatment also caused an increase in LC3-II, stimulated Parkin translocation, and inhibited the expression of p62/SQSTM1 and translocase of outer mitochondrial membrane 20. Therefore, excessive Cr(VI) caused inflammatory damage and mitophagy in chicken liver.
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