High Dietary Organic Iron Supplementation Decreases Growth Performance and Induces Oxidative Stress in Broilers

Abstract

Although Iron (Fe) is an essential nutrient that plays a vital role in respiratory processes, excessive Fe in the diet can affect the health of broilers. We investigated the effects of diet supplemented with high levels of iron chelates with lysine and glutamic acid (Fe–LG) on the growth performance, serum biochemical parameters, antioxidant status, and duodenal mRNA expression of Fe transporters in broilers. A total of 800 1-day-old male Arbor Acres broilers were assigned to 5 groups, with 8 replicates each. Broilers were fed a corn–soybean meal basal diet or basal diets supplemented with 40, 80, 400, or 800 mg Fe/kg as Fe–LG for 6 weeks. The body weight (BW) was increased in the 80 mg Fe/kg treatment group, but decreased in the 800 mg Fe/kg treatment group on day 21. During days 1–21, compared with the control group, the supplementation of the 80 mg Fe/kg increased the average daily gain (ADG) and average daily feed intake (ADFI); however, the supplementation of the 800 mg Fe/kg group decreased the ADG and increased the FCR in broilers (p < 0.05). The heart, liver, spleen, and kidney indices were reduced in the 800 mg Fe/kg treatment group (p < 0.05). The supplementation of the 800 mg Fe/kg group increased the serum aspartate aminotransferase activity and the levels of creatinine and urea nitrogen on day 42 (p < 0.05). The broilers had considerably low liver total superoxide dismutase activity and total antioxidant capacity in the 800 mg Fe/kg treatment group (p < 0.05). Serum and liver Fe concentrations were elevated in the 400 and 800 mg Fe/kg treatment groups, but were not affected in the 40 and 80 mg Fe/kg treatment groups. The duodenal Fe transporters divalent metal transporter 1 (DMT1) and ferroportin 1 (FPN1) were downregulated in the Fe–LG treatment groups (p < 0.05). We conclude that a high dietary supplement of 800 mg Fe/kg in broilers leads to detrimental health effects, causing kidney function injury and liver oxidative stress.

Effects of Iron Oxide Nanoparticle Supplementation on the Growth Performance, Serum Metabolites, Meat Quality, and Jejunal Basal Morphology in Broilers

“…In our study, the serum, liver, and muscle MDA levels were not affected by the IONP supplementation. Our results are in line with the study conducted by Han et al [ 34 ], who reported no changes in the serum and liver MDA levels in broilers supplemented with iron chelated with lysine and glutamine. Iron nanoparticle supplementation decreased the hepatic MDA levels in broilers subjected to heat stress, indicating the antioxidant potential of IONPs, and suggesting the need for IONP supplementation during heat stress conditions [ 28 ].…”

Hybrid Biomimetic Membrane Coated Particles-Mediated Bacterial Ferroptosis for Acute MRSA Pneumonia

“…Similarly, glutamate can prevent ferroptosis by chelating iron. 45 In addition, exogenous GSH supplementation can alleviate the depletion of GSH, play an antioxidant role, and slow down the process of ferroptosis to a certain extent. 18 Ferrostatin-1 is a synthetic antioxidant, which can prevent the damage of the membrane lipid through the reduction mechanism, ultimately restraining ferroptosis.…”

“…Adenosine triphosphate (ATP), adenosine diphosphate (ADP), and tris­(2-carboxyethyl) phosphine (TCEP) have been proved to be able to adsorb iron, resulting in a deficiency of iron, which is indispensable in ferroptosis, and thereby inhibiting ferroptosis and weakening the bactericidal effect. Similarly, glutamate can prevent ferroptosis by chelating iron . In addition, exogenous GSH supplementation can alleviate the depletion of GSH, play an antioxidant role, and slow down the process of ferroptosis to a certain extent .…”

Dietary contribution of iron from limestone and dicalcium phosphate for broiler chickens

“…Increased hepatic ferritin expression suggests that this is the major storage protein of Fe ( Basclain et al, 1998 ), and, therefore, the parallel increases of ferritin and liver Fe are expected. It seems that an upper limit for Fe storage in the liver is out of range in commercial type diets ( Ma et al, 2016 ; Akter et al, 2017 ; Han et al, 2022 ).…”