Protective role of vitamin E on nickel and/or chromium induced oxidative stress in the mouse ovary

Rao, Mandava V; Chawla, Sunita; Sharma, Seema R.

doi:10.1016/j.fct.2009.03.018

Cited by 43 publications

(44 citation statements)

References 32 publications

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“…LPO constitutes a complex chain reaction of free radicals, which may contribute to tissue injury. In this study, NiCl 2 increases MDA contents in the bursa, which is in agreement with the findings in mouse ovary and human B lymphoblastoid cells [48,49]. MDA is a representative product of LPO metabolism, changes the permeability and liquid of cell membrane, and finally leads to oxidative damage of the body [50].…”

Section: Discussionsupporting

confidence: 91%

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: 91%

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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“…In this study, NiCl 2 increased MDA contents in the kidney, which was in agreement with the findings in mouse ovary and human B lymphoblastoid cells [24,25]. MDA is a representative product of LPO metabolism, and its content directly reflects lipid peroxidation damage degree [26].…”

Section: Discussionsupporting

confidence: 89%

NiCl2-Down-Regulated Antioxidant Enzyme mRNA Expression Causes Oxidative Damage in the Broiler’s Kidney

Guo¹,

Wu²,

Cui

et al. 2014

Biol Trace Elem Res

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The kidney serves as a major organ of nickel (Ni) excretion and is a target organ for acute Ni toxicity due to Ni accumulation. There are no studies on the Ni or Ni compound-regulated antioxidant enzyme mRNA expression in animals and human beings at present. This study was conducted to investigate the pathway of nickel chloride (NiCl2)-caused renal oxidative damage by the methods of biochemistry, quantitative real-time polymerase chain reaction, and enzyme-linked immunosorbent assay. 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. Dietary NiCl2 elevated the malondialdehyde (MDA), nitric oxide (NO), 8-hydroxy-2'-deoxyguanosine (8-OHdG) contents, and reduced the ability to inhibit hydroxy radical in the NiCl2-treated groups. Also, the renal inducible nitric oxide synthase (iNOS) activity and mRNA expression levels were increased. The total antioxidant (T-AOC) and activities of antioxidant enzymes including copper zinc superoxide dismutase (CuZn-SOD), manganese superoxide dismutase (Mn-SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), and glutathione-s-transferase (GST) were decreased, and the glutathione (GSH) contents as well were decreased in the kidney. Concurrently, the renal CuZn-SOD, Mn-SOD, CAT, GSH-Px, GST, and GR mRNA expression levels were decreased. The above-mentioned results showed that dietary NiCl2 in excess of 300 mg/kg caused renal oxidative damage by reducing mRNA expression levels and activities of antioxidant enzymes, and then enhancing free radicals generation, lipid peroxidation, and DNA oxidation.

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“…Besides, MDA inhibits various enzyme reactions and exerts mutagenicity and carcinogenicity by forming DNA adducts [36]. The MDA contents were increased in NiCl 2 -treated groups when compared with that in the control group in our study, which were similar to the findings by Rao et al [37] and Lou et al [38], implying that the thymus was undergoing the oxidative stress.…”

Section: Discussionsupporting

confidence: 82%

Effects of Nickel Chloride on Histopathological Lesions and Oxidative Damage in the Thymus

Tang¹,

Li²,

Yin³

et al. 2014

Health

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The purpose of this study was to observe the histopathological lesions and oxidative damage induced by dietary nickel chloride (NiCl 2 ) in the thymus. A total of 280 one-day-old avian broilers were divided into four groups and fed on a corn-soybean basal diet as the control diet or the same basal diet supplemented with 300, 600, and 900 mg/kg of NiCl 2 for 42 days. In the NiCl 2 -treated groups, the broiler weight and thymic relative weight were significantly (P < 0.05 or P < 0.01) decreased. Histopathologically, thymic corpuscles were increased and enlarged; the reticular cells were degenerate and necrotic, and lymphocytes were slightly decreased and loosely arranged in the medulla of thymus in the 600 mg/kg and 900 mg/kg groups. The activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), and the ability to inhibit hydroxy radical and glutathione (GSH) content were significantly (P < 0.05 or P < 0.01) lower in the NiCl2-treated groups than those in the control group, while MDA content was higher. The abovementioned results demonstrated that dietary NiCl 2 in excess of 300 mg/kg could reduce the broiler weight and thymic relative weight, and cause histopathological lesions and oxidative damage in the thymus, which finally impaired the thymic function.

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Protective role of vitamin E on nickel and/or chromium induced oxidative stress in the mouse ovary

Cited by 43 publications

References 32 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

NiCl2-Down-Regulated Antioxidant Enzyme mRNA Expression Causes Oxidative Damage in the Broiler’s Kidney

Effects of Nickel Chloride on Histopathological Lesions and Oxidative Damage in the Thymus

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