Chromium is used in daily life and has a wide range of functions. It plays an important role in
protein synthesis and
carbohydrate and lipid metabolism.
Chromium is found in trivalent Cr(III) and hexavalent
Cr(VI) form; Cr(III) is relatively stable and intimately participates with many phenomena of metabolisms. Whereas,
Cr(VI) is toxic, which results in growth inhibition and leading to changes in components of
antioxidant systems as well as secondary metabolites. However, the molecular mechanism that is involved in
Cr (VI)-induced hepatotoxicity is still unclear. For this purpose, 40 chickens were randomly assigned into two groups: the normal group (feeding the basic diet and clear water), the
chromium group (16%LD50, 74.24 mg/kg/day
K2Cr2O7 ). The samples were subjected to pathological examination and UHPLC-QE-MS non-target metabolomics method for metabolomics analysis of broiler liver using principal component analysis (PCA) and partial least squares discriminant analysis (OPLS-DA). The central venous cells of the broiler liver in the
chromium poisoning group showed turbidity and flaky
necrosis, nuclear condensation, nuclear
rupture, and even nuclear dissolution. The differential metabolite analysis between the
chromium poisoning and the control group showed that 32 differential metabolites were upregulated and 15 were downregulated in positive ion mode. Whereas,17 differential metabolites were downregulated, and 35 were downregulated in negative ion mode (P ≤ 0.05). The potential marker substances are oleic acidamide,
farnesylacetone,
betaine,
taurine,
choline, and
galactinol. Additionally, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways showed that the lipid metabolism, carbohydrate metabolism,
nucleotide metabolism,
amino acid metabolism, energy metabolism, membrane transport, digestive system, and nervous system were the most important metabolic pathways in the liver. This study provides a theoretical basis for the future understanding of the pathogenesis of
chromium poisoning and a new insight of the subsequent molecular mechanism of
chromium hepatotoxicity.