Deficient and excess dietary selenium levels affect growth performance, blood cells apoptosis and liver HSP70 expression in juvenile yellow catfish Pelteobagrus fulvidraco

This study aimed to clarify the effect of selenium (Se) on chromium (VI) [Cr(VI)]-induced damage in chicken liver. A total of 105 chickens were randomly divided into seven groups of 15. Group I received deionized water; group II received Cr(VI) (7.83 mg/kg/d) alone; and other groups orally received both Cr(VI) (7.83 mg/kg/d) and Se of different doses (0.14, 0.29, 0.57, 1.14, and 2.28 mg/kg/d). The levels of superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), Ca -ATPase, and mitochondrial membrane potential (MMP) were measured. Results showed that Cr(VI) increased MDA content and decreased GSH content, T-SOD activity, Ca -ATPase activity, and MMP level. Meanwhile, Se co-treatment (0.14, 0.29, and 0.57 mg/kg/d) increased the viability of the above indicators compared with Cr(VI)-treatment alone. In addition, histopathologic examination revealed that Cr(VI) can cause liver damage, whereas Se supplementation of moderate dose inhibited this damage. This study confirmed that Se exerted protective effect against Cr(VI)-induced liver damage.

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“…Excessive Se (1.14 and 2.28 mg/kg) aggravated liver damage compared with the Cr(VI) treatment alone, Hu et al . and Xu et al .…”

Section: Discussionmentioning

confidence: 99%

Moderate selenium dosing inhibited chromium (VI) toxicity in chicken liver

Wang

Liu

Wan

et al. 2017

J Biochem & Molecular Tox

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“…Normally, dietary selenium level had no effect on survival in fish (Hu et al, ; Liu et al, ). However, uses of plant‐based or low‐vitamin E diet in Atlantic salmon may allow selenium intake leading to immune‐promoting effect and improved survival rate (Berntssen et al, ; Thorarinsson, Landolt, Elliott, Pascho, & Hardy, ).…”

Section: Discussionmentioning

confidence: 99%

“…Selenium is one of the trace elements known as an essential micronutrient for various biological and physiological functions in human and animals, including fish (Hamilton, 2004). Some studies showed that Se deficiency in fish caused growth depression, muscular lesion (Ilham & Fotedar, 2016), oxidative stress, loss of appetite, peroxidative damage and even death (Felton, Landolt, Grace, & Palmisano, 1996;Hu et al, 2016;Poston & Combs, 1979). However, excess amounts of Se may lead to haematological changes (Liu et al, 2018), poor feed efficiency (Pacini et al, 2012), deformities (Lemly, 1993) or toxicity to increase risk of mortality (Hilton, Hodson, & Slinger, 1980).…”

Section: Introductionmentioning

confidence: 99%

Optimum selenium requirement of juvenile Nile tilapia, Oreochromis niloticus

et al. 2019

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A feeding experiment was conducted to determine the optimum selenium requirement in juvenile Nile tilapia. Each of six purified diets with Se‐methionine levels at 0.05, 0.21, 0.41, 0.57, 0.79 and 1.00 mg/kg was assayed in triplicate with initial body weight of 3.00 ± 0.01 g for 8 weeks. The growth of fish was obviously increased when the dietary Se was less than 0.57 mg/kg diet and reached a plateau when the dietary Se was ≥0.57 mg/kg. Serum and hepatopancreatic glutathione peroxidase (GPx) activity increased markedly when the dietary Se was less than 0.57 mg/kg, but then decreased when the dietary Se was higher than 0.57 mg/kg. The malondialdehyde contents in hepatopancreas were significantly decreased when the dietary Se was higher than 0.79 mg/kg. No significant differences were observed in hepatopancreatic total antioxidant capability (T‐AOC) among the groups (p > .05). The results of this study indicated that Se addition as Se‐methionine was essential, while both the deficiency and excess levels of dietary Se would cause negative effects on growth or antioxidant capability in juvenile Nile tilapia. Based on broken‐line regression of WG and piecewise regression of liver GPx, the optimum requirement of Se for juvenile Nile tilapia is 0.57 mg/kg diet.

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“…Krohn et al also found that moderate dietary selenium (from lentil) supplementation (>0.16 mg/kg) is associated with antioxidant defense against arsenic-induced hepatic oxidative stress in mice [ 19 ]. It has also been reported that either deficient or excessive dietary selenium (sodium selenite) cause oxidative stress in the liver of the juvenile yellow catfish Tachysurus fulvidraco [ 20 ]. Therefore, adequate dietary selenium was required for the maintenance of antioxidant enzyme system and helped to prevent hepatic mitochondria oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial Protein Profile in Mice with Low or Excessive Selenium Diets

Wang

Zhang

et al. 2016

IJMS

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Dietary selenium putatively prevents oxidative damage, whereas excessive selenium may lead to animal disorder. In this study, we investigated the effects of low and excessive levels of dietary selenium on oxidative stress and mitochondrial proteins in mouse liver. Six to eight week old mice were fed a diet with low, excessive, or moderate (control) levels of selenium (sodium selenite). The selenium concentration and oxidative stress-related parameters in hepatic mitochondria were evaluated. Two-dimensional electrophoresis and mass spectrometry were applied to identify the differentially-expressed proteins associated with dietary selenium. The selenium content of the livers in mice with the low selenium diet was significantly lower than that of the control, while that of mice fed excessive levels was significantly higher. In both groups oxidative stress in hepatic mitochondria was found; accompanied by lower superoxide dismutase (SOD) and glutathione peroxidase (GPX) levels and higher malondialdehyde (MDA) content, compared with the control group. Furthermore, ten proteins in the hepatic mitochondria of the selenium-low or -excessive groups with more than two-fold differences in abundance compared with the control group were identified. The differentially-expressed proteins in hepatic mitochondria may be associated with dietary (low or excessive) selenium-induced oxidative stress.

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Deficient and excess dietary selenium levels affect growth performance, blood cells apoptosis and liver HSP70 expression in juvenile yellow catfish Pelteobagrus fulvidraco

Cited by 32 publications

References 80 publications

Moderate selenium dosing inhibited chromium (VI) toxicity in chicken liver

Moderate selenium dosing inhibited chromium (VI) toxicity in chicken liver

Optimum selenium requirement of juvenile Nile tilapia, Oreochromis niloticus

Mitochondrial Protein Profile in Mice with Low or Excessive Selenium Diets

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