Effects of Different Doses of Excessive Iron in Diets on Oxidative Stress in Immune Organs of Sheep

Liu, XueJie; Zhao, Jinghua; Zhang, LiangYu; Lu, Jin‐Jian; Lv, Xiaoping; Liu, ChaoNan; Gao, Xueli

doi:10.1007/s12011-019-02006-9

Cited by 7 publications

(8 citation statements)

References 29 publications

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“…The results of the present study showed that iron content in the liver was increased with increasing levels of iron added to the diet, indicating a dose-dependent relationship between body iron content and dietary iron levels. This is consistent with the results of experiments with sheep (Liu et al, 2020). Excessive iron intake can lead to iron deposition, but interestingly, this phenomenon largely returns to normal over a period of time.…”

Section: Discussionsupporting

confidence: 90%

Excess Iron added to the diet induces the apoptosis of chicken’s liver through the PI3KAKT mTOR axis

Sun

et al. 2022

Preprint

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Iron (Fe), an essential trace element, plays a key role in biological metabolism. The PI3K/AKT/mTOR axis plays an important role in the control of apoptosis. However, the effect of iron overdose in the diet on the role of the PI3K/AKT/mTOR axis and apoptosis, and pathological liver damage in chickens are still poorly understood. In this study, 180 1-day-old chicks were divided into 3 groups, which were fed the basal diets supplemented with 50 (C), 500 (E1), and 1000 (E2) mg Fe/Kg as ferrous sulfate monohydrate (FeSO4·H2O) and returned to normal diet one day later, Tested on days 1, 3, 7, 14, and 21 after the end of the iron addition. The results showed that the liver morphology was normal in the group C. The groups E1 and E2 showed the structure destroyed of hepatic lobules, the disordered of hepatic cords, the reduction of the central veins and the presence of erythrocytes accompanied by inflammatory cell infiltration. The group E2 showed more serious damage than the group E1, but these phenomena will largely return to normal on day 21. The perls staining showed that large deposits of iron-containing hemosiderin in the hepatic sinus after iron overdose intake, and the changes of iron deposition and pathological damage had certain regularity in time. The expression of Bax, Caspase-3, Caspase-8, and Caspase-9 in groups E1 and E2 were increased from days 1 to 21, which was in contrast to the Bcl-2, and it has a dose dependent. This suggested that iron overdose triggered apoptosis, which was supported by our ultrastructural observations of chromatin marginalization and impaired mitochondrial swelling. In addition, the expression of PI3K and AKT were significantly increased in the iron overdose groups, while the expression of mTOR was decreased. Above all, iron overdose can induce apoptosis in chicken hepatocytes through regulation of the PI3K/AKT/mTOR axis, leading to pathological damage. The type of iron overdose-induced damage was dose-dependent but not permanent. These results provide a theoretical basis for a comprehensive understanding of the importance of mineral nutrition management in poultry and the possible risk of excessive iron intake.

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Section: Discussionsupporting

confidence: 90%

Excess Iron added to the diet induces the apoptosis of chicken’s liver through the PI3KAKT mTOR axis

Sun

et al. 2022

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“…2,3 At the other end of the spectrum, iron overload could lead to increased reactive oxygen species (ROS) damaging T-and B-lymphocytes, and potentially increase the risk of adverse respiratory conditions. 4,5 Previous human cohort studies showed that lower maternal hemoglobin or hematocrit concentrations during pregnancy were associated with a lower forced vital capacity (FVC) at the age of 8-9 years, 6 a higher risk of wheeze at the age of 1 year, and a higher risk of asthma at the age of 6 years of the children. 7 We previously demonstrated that a higher maternal hematocrit during pregnancy was associated with a lower forced expiratory flow at 75% of forced vital capacity (FEF 75 ) in children at the age of 10 years.…”

Section: Introductionmentioning

confidence: 99%

Maternal hemoglobin and iron status in early pregnancy and risk of respiratory tract infections in childhood: A population‐based prospective cohort study

Quezada‐Pinedo,

van Meel,

Reiss

et al. 2023

Pediatric Allergy Immunology

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BackgroundMaternal hemoglobin and iron status measures during pregnancy might affect the developing fetal respiratory system leading to adverse respiratory conditions. Our aim was to assess the associations of maternal hemoglobin and iron status measures during pregnancy with the risk of respiratory tract infections in children until 10 years of age.MethodsIn a population‐based cohort study among 5134 mother–child pairs, maternal hemoglobin and iron status including ferritin, transferrin, and transferrin saturation were measured during early pregnancy. In children, physician‐attended respiratory tract infections from age 6 months until 10 years were assessed by questionnaires. Confounder‐adjusted generalized estimating equation modeling was applied.ResultsAfter taking multiple testing into account, high maternal ferritin concentrations and low maternal transferrin saturation during pregnancy were associated with an overall increased risk of upper, not lower, respiratory tract infections until age 10 years of the child [OR (95% CI: 1.23 (1.10, 1.38) and 1.28 (1.12, 1.47), respectively)]. High maternal transferrin saturation during pregnancy was associated with a decreased and increased risk of upper respiratory tract infections at 1 and 6 years, respectively, [OR (95% CI: 0.60 (0.44, 0.83) and 1.54 (1.17, 2.02))]. Observed associations were suggested to be U‐shaped (p‐values for non‐linearity ≤.001). Maternal hemoglobin and iron status measures during pregnancy were not consistently associated with child's gastroenteritis and urinary tract infections, as proxies for general infection effects.ConclusionHigh maternal ferritin and low transferrin saturation concentrations during early pregnancy were most consistently associated with an overall increased risk of child's upper, not lower, respiratory tract infections.

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“…It also participates in the activation and regulation of immune system, and the proliferation and differentiation of immune cells [5]. According to the research announced by National Research Council (NRC), sheep has the least tolerance to iron compared with other livestock [6].The risk of toxicosis will increase if maximum dose of iron is provided [7]. Iron is transported to all parts of the body via blood circulation and widely distributed in sorts of tissues and organs [8].Therefore, excess iron will cause renal anemia, liver disease, cardiovascular disease, and nerve damage.…”

Section: Introductionmentioning

confidence: 99%

“…The relationship between iron and immune function has been concerned, particularly in related to the underlying in ammatory process found in diseases with chronic immune stimulation [17,20]. The skeletal muscle produces and releases IL-6, which can increase the concentration of blood hepcidin [7]. P. Huang has found that IL-6 and TNF-α can promote hepcidin for accelerating iron metabolic homeostasis and improve the expression of TfR224.…”

Section: Introductionmentioning

confidence: 99%

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Disorders of Major Inflammatory Factors and Histopathological Lesions in Excess-iron-fed Sheep Liver

Zhang¹,

Lu²,

Sun³

et al. 2021

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Background: Iron plays a key role in biological metabolism as an essential microelement. Excess iron may cause pathological damage to the body. The purpose of this work is to explore the disorders of major inflammatory factors and histopathological lesions in the liver of excess-iron-fed sheep. Twenty German Mutton Merino sheep were randomly divided into 4 groups, control group (CON), iron-excess group one (IronE1), iron-excess group two (IronE2) and iron-excess group three (IronE3), respectively. Each group was fed with basal diets supplemented with 50 (CON), 500 (IronE1), 1000 (IronE2), and 1500 (IronE3) mg/kg as ferrous sulfate monohydrate (FeSO4 ·H2O). After 75 days, the liver was removed and collected. A variety of methods were utilized to detect indicators of sheep liver. Results: The histopathological damage of liver in sheep was rather severe with the excess of iron. Hemosiderin deposits were also obviously discovered. The results also showed that the expression of both protein and mRNA of IL-1β, TNF-α and IFN-γ reduced, but the factors of IL-2, IL-6, NF-κB and TGF-β1 obviously increased in the liver of each iron excess group. Corresponding changes were also discovered with the addition of iron dosage. The content of inflammatory factors above showed a significant change with an addition of 1500 mg/kg iron into the basic diet, which indicated that excess iron inhibited the release of IL-1β, TNF-α and IFN-γ in the sheep liver. The inflammation caused by excess iron extenuated by reducing the content of these three pro-inflammatory factors. The expression of IL-2, IL-6, NF-κB and TGF-β1 increased. As pro-inflammatory factors induced inflammation, anti-inflammatory factors also increased to protect the body from tissue damage. Conclusions: It can be concluded that excess iron can change the expression of main inflammatory factors in sheep liver, which will be an instructive significance to the development of medical prospect for sheep breeding and disease diagnosis.

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Effects of Different Doses of Excessive Iron in Diets on Oxidative Stress in Immune Organs of Sheep

Cited by 7 publications

References 29 publications

Excess Iron added to the diet induces the apoptosis of chicken’s liver through the PI3KAKT mTOR axis

Excess Iron added to the diet induces the apoptosis of chicken’s liver through the PI3KAKT mTOR axis

Maternal hemoglobin and iron status in early pregnancy and risk of respiratory tract infections in childhood: A population‐based prospective cohort study

Disorders of Major Inflammatory Factors and Histopathological Lesions in Excess-iron-fed Sheep Liver

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