Protection of Selenium on Hepatic Mitochondrial Respiratory Control Ratio and Respiratory Chain Complex Activities in Ducklings Intoxicated with Aflatoxin B1

Shi, Dayou; Guo, Shining; Liao, Shenquan; Su, Rongsheng; Guo, Mingsheng; Liu, Nian; Li, Pengfei; Tang, Zhaoxin

doi:10.1007/s12011-011-9195-6

Cited by 17 publications

(15 citation statements)

References 23 publications

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“…Humans are exposed to these metals from numerous sources, including contaminated air, water, soil, and food. Selenium has been shown to alter heavy metal toxicity specially mercury which cause adverse effects on the various tissue parameters [15,24,31,[47][48][49][50][51][52][53][54].…”

Section: Discussionmentioning

confidence: 99%

Effect of Selenium on the Levels of Cytokines and Trace Elements in Toxin-Mediated Oxidative Stress in Male Rats

Ansar

2015

Biol Trace Elem Res

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Selenium is an essential cofactor in the key enzymes involved in cellular antioxidant defense. This study was designed to investigate the protective effects of selenium on mercury chloride (HgCl2)-induced toxicity. Male Wistar rats were randomly divided into four groups of six animals each. The first group was control; the second group was treated with mercuric chloride (HgCl2: 50 mg/kg/bw). The third group was treated with sodium selenite (Se 0.2 mg/kg/bw), and the fourth group received Se (0.2 mg/kg/bw) plus HgCl2 (50 mg/kg for 24 h). The influence of Se on mercury induced levels of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) and zinc, copper, and iron in serum of rats were observed. The serum MDA, SOD, zinc, and iron concentrations were found to be statistically different among the control and toxin-treated group. The serum levels of IL-6, IL-10, and TNF-α were also measured. There was a significant decrease in the levels of TNF-α, IL-6, and IL-10 in toxin-treated group II compared with that of the control group (p < 0.05). A significant increase in the serum levels of inflammatory cytokines IL-6, TNF-α, and IL-10 after administration of Se seemed to counteract some of the damage, as indicated by differences in the serum concentrations of major elements.

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Section: Discussionmentioning

confidence: 99%

Effect of Selenium on the Levels of Cytokines and Trace Elements in Toxin-Mediated Oxidative Stress in Male Rats

Ansar

2015

Biol Trace Elem Res

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“…Accumulation of ROS and downregulation of physiological antioxidant has a dual effect of oxidative stress. Aflatoxin B 1 was found to act through this way in ducklings . Molecular pathways of mitochondrial dysfunction and cellular events are shown in Fig.…”

Section: Discussionmentioning

confidence: 89%

“…Treatment of 7‐day‐old ducklings with aflatoxin B1, a potent carcinogen produced by HYPERLINK “https://en.wikipedia.org/wiki/Aspergillus_flavus“\o “Aspergillus flavus” Aspergillus flavus and HYPERLINK “https://en.wikipedia.org/wiki/A._parasiticus“\o “A. parasiticus” A. parasiticus (0.1 mg/kg body weight), significantly increased the activity of hepatic mitochondrial complexes I‐IV and induced hepatic mitochondrial respiratory dysfunction . It also decreased the activity of hepatic mitochondrial enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH‐Px), GR, and mitochondrial malondialdehyde (MDA), along with a significant induction of mitochondrial antioxidant dysfunction in ducklings .…”

Section: Resultsmentioning

confidence: 99%

Mycotoxin‐assisted mitochondrial dysfunction and cytotoxicity: Unexploited tools against proliferative disorders

et al. 2018

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Mitochondria are the powerhouse of cells, which upon dysfunctions may lead to several diseases. Mycotoxins are the toxic secondary metabolites from fungi which are capable of causing diseases and death in humans and animals. They have a versatile mechanism of action in biological systems and can be used as lead compounds to treat some diseases including cancer. The present work encompasses analysis on the effects of mycotoxins on mitochondrial dysfunction. Electronic databases such as PubMed, ScienceDirect, Scopus, Web of Science, and Google Scholar were thoroughly searched for up-to-date published information associated with those mycotoxins and their effect on mitochondrial dysfunction. Findings suggest that mycotoxins such as citrinin, aflatoxin, and T-2 toxin exert multi-edged sword-like effects in test systems causing mitochondrial dysfunction. Mycotoxins can induce oxidative stress even at low concentration/dose that may be one of the major causes of mitochondrial dysfunction. On the other hand, activation of apoptotic caspases and other proteins by mycotoxins may lead to apoptotic cell death. Thus, mycotoxins-mediated mitochondrial dysfunction may be related to several chronic diseases which also makes these mycotoxins considerable as lead compounds for inducing toxic effects in cells. Their cytotoxic effects on cancer cells suggest their possible application as chemotherapeutic tools. © 2018 IUBMB Life, 70(11):1084-1092, 2018.

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“…Indeed, ROS caused by aflatoxins are considered to be main mechanisms leading to hepatotoxicity . Recent reports indicated that antioxidant natural components have potential role on AFB1‐induced oxidative toxicity in animal models although their protective results on the toxicity are conflicting …”

Section: Introductionmentioning

confidence: 99%

“…6 Recent reports indicated that antioxidant natural components have potential role on AFB1-induced oxidative toxicity in animal models although their protective results on the toxicity are conflicting. 2,7,8 Liver protectors have often been detected when studying the effect of substances purified from extracts of natural products to which folk medicine has attributed therapeutic properties. Caffeic acid phenethyl ester (CAPE) is a flavonoid-like compound and an active component of propolis from honeybee hives and it has been used in traditional medicine in the Far East for decades.…”

Section: Introductionmentioning

confidence: 99%

Caffeic acid phenethyl ester modulates aflatoxin B1‐induced hepatotoxicity in rats

Akçam

Artan

Yılmaz

et al. 2013

Cell Biochemistry & Function

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Aflatoxin B1 (AFB1) is the most potent of the mycotoxins and is widely observed in nutrition abnormalities. There are some studies suggesting oxidative stress-induced toxic changes on liver related to AFB1 toxicity. The aim of the present study was to evaluate whether antioxidant caffeic acid phenethyl ester (CAPE) relieves oxidative stress in AFB1-induced liver injury in rat. Twenty-four male rats were equally divided into three groups. The first group was used as a control. The second group received three doses of AFB1. The three doses of CAPE were given to constitute the third group with doses of AFB1. After 10 days of experiment, liver and serum samples were taken from all animals. Serum gamma glutamyl transferase (GGT), alkaline phosphatase (ALP), glutathione s-transferase (GST), nitric oxide (NO) and sulfhydryl values were higher in the AFB1 group than in control, whereas serum GGT, ALP, GST and NO values were decreased by in the AFB1 + CAPE group than in AFB1 group. Liver GST, total oxidant capacity, sulfhydryl, apoptosis index and ischemia-modified albumin values were higher in the AFB1 group than in control, whereas the GST activity and apoptosis index were lower in the AFB1 + CAPE group than in the AFB1 group. There were histopathological degeneration and apoptosis in hepatocytes of AFB1 group. The findings were totally recovered by CAPE administration. In conclusion, we observed that AFB1 caused oxidative and nitrosative hepatoxicity to hepatocytes in the rat. However, CAPE induced protective effects on the AFB1-induced hepatoxicity by modulating free radical production, biochemical values and histopathological alterations.

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Protection of Selenium on Hepatic Mitochondrial Respiratory Control Ratio and Respiratory Chain Complex Activities in Ducklings Intoxicated with Aflatoxin B1

Cited by 17 publications

References 23 publications

Effect of Selenium on the Levels of Cytokines and Trace Elements in Toxin-Mediated Oxidative Stress in Male Rats

Effect of Selenium on the Levels of Cytokines and Trace Elements in Toxin-Mediated Oxidative Stress in Male Rats

Mycotoxin‐assisted mitochondrial dysfunction and cytotoxicity: Unexploited tools against proliferative disorders

Caffeic acid phenethyl ester modulates aflatoxin B1‐induced hepatotoxicity in rats

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