This experiment fed broiler chickens boric acid at 120 or 240 mg/kg dietary boron for 7 or 14 days and studied liver injury, with parallel experiments in cultured chicken embryo hepatocytes. Boron accumulated in liver, raised serum ALT and AST, caused dose- and time-dependent histological and mitochondrial damage, and shifted gene and protein markers toward oxidative stress and ferroptosis. A ferroptosis inhibitor reduced the damage in cells.
Key numbers
- Diet groups: 0, 120 and 240 mg/kg boron as boric acid; drinking water boron below 0.5 ppm (Methods, Section 2).
- Hepatocyte exposure: up to 80 mM boron, stated as the IC50, for 24 hours (Methods).
- Liver and serum boron rose in all treated groups versus control (P < 0.05); values are shown only in Figure 1, so no concentrations are recorded here (Results 3.1).
Methods (brief)
Sixty broilers were randomized to three diet groups for 7 or 14 days; liver boron was measured by ICP-OES, serum ALT and AST, histology and electron microscopy, transcriptomics, and Western blots for ferroptosis markers. Chicken embryo hepatocytes were treated with boron with or without ferrostatin-1 or erastin.
Evidence fitness
Supports a mechanistic finding that high dietary boron injures poultry liver through oxidative stress and ferroptosis. It does not support human exposure estimates, poultry product concentrations or human dose-response.
Limitations
Short exposures at high doses; tissue concentrations only shown graphically; n = 5 per group in some analyses. Funded by the Guangdong Basic and Applied Basic Research Foundation; no conflicts declared.
Related evidence
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