Antioxidant system efficiently protects goldfish gills from Ni2+-induced oxidative stress

Kubrak, Olga I.; Husak, Viktor V.; Rovenko, Bohdana M.; Poigner, Harald; Kriews, Michael; Abele, Doris; Lushchak, Volodymyr I.

doi:10.1016/j.chemosphere.2012.06.044

Cited by 48 publications

(10 citation statements)

References 45 publications

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“…**p < 0.01, compared with the control group or lesions [18][19][20][21][22]. Some studies have reported that NiCl 2 can decrease the activities of enzymic and non-enzymic antioxidants in rats, Tigriopus japonicus Mori, and goldfish [39][40][41]. Also, our data are consistent with the report that NiSO 4 can decrease the SOD and CAT activities in the liver of mouse [42].…”

Section: Discussionsupporting

confidence: 95%

Nickel Chloride (NiCl2) Induces Histopathological Lesions via Oxidative Damage in the Broiler’s Bursa of Fabricius

Yin¹,

Guo²,

Cui

et al. 2015

Biol Trace Elem Res

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The purpose of this study was to investigate the histopathological lesions, oxidative damage, changes of immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) contents in the bursa of Fabricius and serum immunoglobulins (IgG, IgM, IgA) induced by dietary nickel chloride (NiCl2). Two hundred and eighty-one-day-old broilers were randomly divided into four groups and fed on a control diet and three experimental diets supplemented with 300, 600, and 900 mg/kg of NiCl2 for 42 days. Lesions were observed in the NiCl2-treated groups. Histopathologically, lymphocytes were decreased in lymphoid follicles with thinner cortices and wider medullae. Concurrently, the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and the ability to inhibit hydroxyl radical and glutathione (GSH) contents were significantly (p < 0.05 or p < 0.01) decreased, while malondialdehyde (MDA) contents were increased in the NiCl2-treated groups. The serum IgG, IgM, and bursa IgG and IgM contents were significantly (p < 0.05 or p < 0.01) lower in the NiCl2-treated groups than those in the control group. The above-mentioned results show that dietary NiCl2 in excess of 300 mg/kg can cause histopathological lesions via oxidative damage, which finally impairs the function of the bursa of Fabricius and reduces IgG and IgM contents of the serum and the bursa of Fabricius. The study is aimed to provide helpful materials for studies on Ni- or Ni compounds-induced B cell toxicity in both human and other animals in the future.

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Section: Discussionsupporting

confidence: 95%

Nickel Chloride (NiCl2) Induces Histopathological Lesions via Oxidative Damage in the Broiler’s Bursa of Fabricius

Yin¹,

Guo²,

Cui

et al. 2015

Biol Trace Elem Res

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“…However, symptoms of toxicity can occur when too much Ni is taken up [ 3 ]. Ni is potentially hazardous to living organisms due to its genotoxicity, immunotoxicity, mutagenicity and cancinogenicity [ 5 , 6 , 7 ]. Exposure of workers to Ni compounds can produce adverse effects on their health, such as Ni allergy, contact dermatitis, lung fibrosis, cardiovascular diseases, kidney diseases, and cancer of the respiratory tract [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Modulation of the PI3K/Akt Pathway and Bcl-2 Family Proteins Involved in Chicken’s Tubular Apoptosis Induced by Nickel Chloride (NiCl2)

Guo

Cui

Peng

et al. 2015

IJMS

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Exposure of people and animals to environments highly polluted with nickel (Ni) can cause pathologic effects. Ni compounds can induce apoptosis, but the mechanism and the pathway of Ni compounds-induced apoptosis are unclear. We evaluated the alterations of apoptosis, mitochondrial membrane potential (MMP), phosphoinositide-3-kinase (PI3K)/serine-threonine kinase (Akt) pathway, and Bcl-2 family proteins induced by nickel chloride (NiCl2) in the kidneys of broiler chickens, using flow cytometry, terminal deoxynucleotidyl transferase 2ʹ-deoxyuridine 5ʹ-triphosphate dUTP nick end-labeling (TUNEL), immunohistochemstry and quantitative real-time polymerase chain reaction (qRT-PCR). We found that dietary NiCl2 in excess of 300 mg/kg resulted in a significant increase in apoptosis, which was associated with decrease in MMP, and increase in apoptosis inducing factor (AIF) and endonuclease G (EndoG) protein and mRNA expression. Concurrently, NiCl2 inhibited the PI3K/Akt pathway, which was characterized by decreasing PI3K, Akt1 and Akt2 mRNA expression levels. NiCl2 also reduced the protein and mRNA expression of anti-apoptotic Bcl-2 and Bcl-xL and increased the protein and mRNA expression of pro-apoptotic Bax and Bak. These results show that NiCl2 causes mitochondrial-mediated apoptosis by disruption of MMP and increased expression of AIF and EndoG mRNA and protein, and that the underlying mechanism of MMP loss involves the Bcl-2 family proteins modulation and PI3K/Akt pathway inhibition.

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“…Several studies have demonstrated changes in ROS and T-AOC in the gills of fish as a result of exposure to heavy metals, pesticides, and other toxicants Kubrak et al, 2013). However, few data are available regarding the effects of exposure to cyanobacterial neurotoxins or PSPs on ROS and T-AOC in fish gills.…”

Section: Changes In Ros and T-aoc In The Gills Of Aphantoxin-exposed mentioning

confidence: 99%

In vivo effects of Aphanizomenon flos-aquae DC-1 aphantoxins on gas exchange and ion equilibrium in the zebrafish gill

et al. 2016

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Antioxidant system efficiently protects goldfish gills from Ni2+-induced oxidative stress

Cited by 48 publications

References 45 publications

Nickel Chloride (NiCl2) Induces Histopathological Lesions via Oxidative Damage in the Broiler’s Bursa of Fabricius

Nickel Chloride (NiCl2) Induces Histopathological Lesions via Oxidative Damage in the Broiler’s Bursa of Fabricius

Modulation of the PI3K/Akt Pathway and Bcl-2 Family Proteins Involved in Chicken’s Tubular Apoptosis Induced by Nickel Chloride (NiCl2)

In vivo effects of Aphanizomenon flos-aquae DC-1 aphantoxins on gas exchange and ion equilibrium in the zebrafish gill

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