Mechanism of cadmium-induced cytotoxicity in rat hepatocytes: cadmium-induced active oxygen-related permeability changes of the plasma membrane

Koizumi, Toshiaki; Shirakura, Hiroaki; Kumagai, Hiroshi; Hideki, Tatsumoto; Suzuki, Kazuo

doi:10.1016/s0300-483x(96)03477-4

Cited by 101 publications

(50 citation statements)

References 39 publications

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“…In the present study, the oxidative insult of Cd increased the MDA level, an oxidative product of LPO in brain tissue. Previous studies suggest that Cd-induced lipid peroxidation is due to the generation of hydroxyl radicals, superoxide anions, nitric oxide and H 2 O 2 (55)(56)(57). Indeed, in the present study, treatment with CA effectively reduced the MDA level and this may be due to the ability of CA to transfer electrons, scavenge free radicals, chelate metals and activate antioxidant enzymes.…”

Section: Discussionsupporting

confidence: 61%

Therapeutic efficacy of chlorogenic acid on cadmium-induced oxidative neuropathy in a murine model

Hao

Pan

Zhang

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. The aim of the present study was to determine whether chlorogenic acid (CA) is able to modulate cadmium (Cd)-induced oxidative brain damage. Cd-treated rats displayed numerous pathological effects, including the inhibition of acetylcholinesterase, elevated lipid peroxidation, the depletion of enzymatic and non-enzymatic antioxidants, the reduction of membrane-bound ATPase activity, mitochondrial dysfunction and DNA fragmentation. Pretreatment of the rats with CA significantly attenuated these effects. These results lead to the hypothesis that the mechanisms by which CA attenuates the effects of Cd-induced oxidative brain damage include the maintenance of antioxidant homeostasis, inhibition of the membrane effects and the perpetuation of mitochondrial dysfunction. These data support the potential of CA as a beneficial intervention in the prevention of heavy metal poisoning due to Cd exposure.

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Section: Discussionsupporting

confidence: 61%

Therapeutic efficacy of chlorogenic acid on cadmium-induced oxidative neuropathy in a murine model

Hao

Pan

Zhang

et al. 2015

Experimental and Therapeutic Medicine

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“…Additionally, a significant positive linear correlation (r = 0.45256; P < 0.0001) was detected between LDH and PI flow cytometry assays used in the current study. Other studies have also reported a linear correlation between the LDH release and PI uptake in Madin-Darby canine kidney (MDCK) cells exposed to mercuric chloride (HgCl 2 ) (Gores et al, 1988) and in hepatocytes exposed to cadmium (Cd) (Koizumi et al, 1996). The extent of membrane damage was reported by Liao et al (2011) to be related to variations in membrane components (i.e.…”

Section: Discussionmentioning

confidence: 94%

Characterization of cell death caused by diplodiatoxin and dipmatol, toxic metabolites of Stenocarpella maydis

Masango

Ellis

Botha

2015

Toxicon

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Highlights• Diplodiatoxin and dipmatol induced necrosis in Neuro-2a, CHO-K1 and MDBK cells.• Diplodiatoxin and dipmatol induced caspase-dependent apoptosis in vitro.• Mitochondrial damage, cytoplasmic vacuoles and nuclear fragmentation were observed. AbstractDiplodiosis, a neuromycotoxicosis of cattle and sheep grazing on mouldy cobs infected by Stenocarpella maydis, is considered the last major veterinary mycotoxicosis for which the causative mycotoxin is still unknown. The current study was aimed at characterizing the cell death observed in mouse neuroblastoma (Neuro-2a), Chinese hamster ovary (CHO-K1) and Madin-Darby bovine kidney (MDBK) cell lines exposed to the S. maydis metabolites (i.e. diplodiatoxin and dipmatol) by investigating the roles of necrosis and apoptosis. Necrosis was investigated using the lactate dehydrogenase (LDH) leakage and propidium iodide (PI) flow cytometry assays and apoptosis was evaluated using the caspase-3/7 and Annexin V flow cytometry assays. In addition, transmission electron microscopy (TEM) was used to correlate the cell death pathways observed in this study with their typical morphologies. Both diplodiatoxin and dipmatol (750 μM) induced necrosis and caspase-dependent apoptosis in Neuro-2a, CHO-K1 and MDBK cells. Ultrastructurally, the two mycotoxins induced mitochondrial damage, cytoplasmic vacuolation and nuclear fragmentation in the three cell lines. These findings have laid a foundation for future studies aimed at elucidating in detail the mechanism of action of the S. maydis metabolites.

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“…SOD, U·mL oxidative damage to the brain, heart, kidneys, and reproductive organs with neurological, haematological, gastrointestinal, reproductive, circulatory, and immunological pathologies (Koizumi et al 1996;Ercal et al 2001;Valko et al 2005). Transition metals act as catalysts in the oxidative reactions of biological macromolecules and deplete cells' major antioxidants, particularly thiol-containing antioxidants and enzymes.…”

Section: Discussionmentioning

confidence: 99%

Blood oxidative stress and antioxidant defense profile of White Stork Ciconia ciconia chicks reflect the degree of environmental pollution

Tkachenko¹,

Kurhaluk²

2014

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Abstract. Oxidative stress biomarkers in the blood of White Stork Ciconia ciconia chicks were analyzed during their development in nests in polluted and control environments. The control, relatively pure, environment was the village of Kłopot, with no industrial plants within a radius of 150 km. Blood samples were also collected in two polluted areas, including the suburban village of Czarnowo, located 20 km from the city of Zielona Góra (southwestern Poland) and an area near the town of Głogów, where a large Copper Manufacture is situated. We measured two markers of oxidative stress (2-thiobarbituric acid reactive substances (TBARS) and stable 2,4-dinitrophenyl hydrazine derivates of the oxidative modified carbonyl groups levels), as well as antioxidant defenses (superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase activities, ceruloplasmin and total antioxidant capacity levels) in the blood samples. White Stork chicks from different environments are probably significantly susceptible to environmental conditions. In the unpolluted area, chicks showed lower lipid and protein oxidation levels, indicating that the variation in the pollution-induced oxidative stress among areas is dependent of environmental loads. Increased oxidative stress biomarkers can modify antioxidant defenses in chicks from various environments, principally causing increased glutathione peroxidase activity in chicks from polluted regions. Therefore, the use of oxidative stress biomarkers to assess the health and condition of chicks will be useful in future studies aiming to identify miscellaneous environmental loading.

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Mechanism of cadmium-induced cytotoxicity in rat hepatocytes: cadmium-induced active oxygen-related permeability changes of the plasma membrane

Cited by 101 publications

References 39 publications

Therapeutic efficacy of chlorogenic acid on cadmium-induced oxidative neuropathy in a murine model

Therapeutic efficacy of chlorogenic acid on cadmium-induced oxidative neuropathy in a murine model

Characterization of cell death caused by diplodiatoxin and dipmatol, toxic metabolites of Stenocarpella maydis

Blood oxidative stress and antioxidant defense profile of White Stork Ciconia ciconia chicks reflect the degree of environmental pollution

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