biphenyl/necrosis

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Ukurasa 1 kutoka 138 matokeo

Comparative toxicologic study with polychlorinated biphenyls in chickens with special reference to porphyria, edema formation, liver necrosis, and tissue residues.

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Ingia / Ingia

[Prevention by metyrapone of halothane induced liver necrosis in rats (author's transl)].

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Ingia / Ingia

Liver necrosis and an increase of serum sorbitol dehydrogenase activity can be produced in rats by halothane anesthesia (1% v/v in oxygen) following pretreatment with polychlorinated biphenyls. Using this model, it was shown that administration of metyrapone (2-methyl-1,2-bis(3-pyridyl)-1-propanone)

[PCBs cause necrosis of L6C5 myoblasts].

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Ingia / Ingia

Polychlorinated biphenyls (PCBs) are structurally related to dioxins, widely used in the past in various industrial applications and daily used products. Although PCBs production was discontinued more than twenty years ago, their chemical stability and high lipophilicity make them persistent

A novel cyclin-dependent kinase inhibitor down-regulates tumor necrosis factor-alpha (TNF-alpha)-induced expression of cell adhesion molecules by inhibition of NF-kappaB activation in human pulmonary epithelial cells.

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Ingia / Ingia

BAI (a novel cyclin-dependent kinase (CDK) inhibitor, 2-[1,1'-biphenyl]-4-yl-N-[5-(1,1-dioxo-1lambda(6)-isothiazolidin-2-yl)-1H-indazol-3-yl] acetamide) is known to have anti-proliferative activity, but the mechanism responsible for it remains unclear. We here investigated the functional effect of

Liver morphology in guinea pigs fed pyrolysis products of a polychlorinated biphenyl transformer fluid continuously for 90 days.

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Ingia / Ingia

After a fire involving a transformer, the State Office Building in Binghamton, New York, was contaminated with soot containing polychlorinated biphenyls, biphenylenes, naphthalenes, dioxins, and dibenzofurans. The toxicity of the soot and its effect on liver morphology after prolonged (subchronic)

Cell death mechanisms in AtT20 pituitary cells exposed to polychlorinated biphenyls (PCB 126 and PCB 153) and methylmercury.

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Ingia / Ingia

Polychlorinated biphenyls (PCBs) are persistent food contaminants that can have adverse effects on the endocrine and nervous systems, including the pituitary. In the present study, we have investigated cell death in the AtT20 pituitary cell line after exposure to coplanar PCB 126 and non-coplanar

Polychlorinated biphenyl 138 exposure-mediated lipid droplet enlargement endows adipocytes with resistance to TNF-α-induced cell death.

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Ingia / Ingia

Although epidemiological reports have shown the association between polychlorinated biphenyls (PCBs) and obesity, the molecular mechanism of PCB-induced obesity is mostly unknown. The aim of the present study was to further dissect the significance of lipid droplet (LD) enlargement in PCB-induced

Exercise influences the impact of polychlorinated biphenyl exposure on immune function

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Ingia / Ingia

Polychlorinated biphenyls (PCBs) are environmental pollutants and endocrine disruptors, harmfully affecting reproductive, endocrine, neurological and immunological systems. This broad influence has implications for processes such as wound healing, which is modulated by the immunological response of

Non-dioxin-like polychlorinated biphenyls (PCB 101, PCB 153 and PCB 180) induce chondrocyte cell death through multiple pathways.

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Ingia / Ingia

Environmental pollutants are known to have adverse effects on human health. However, the link between chemical exposure and osteoarthritis remains little investigated. This study sought to assess in vitro the effect of several non-dioxin-like polychlorinated biphenyls (NDL-PCBs) on chondrocytes

Relationship of polychlorinated biphenyls with type 2 diabetes and hypertension.

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Ingia / Ingia

Diabetes and hypertension are important contributors to morbidity and mortality worldwide. Both of these conditions are caused by some combination of genetic and environmental factors which may include exposure to persistent organic pollutants (POPs) such as polychlorinated biphenyls (PCBs). Studies

Tissue distribution of polychlorinated biphenyls (Aroclor 1254) in cockerels: relation to the duration of exposure and observations on pathology.

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Ingia / Ingia

Day old cockerels were given a ration containing 500 ppm of polychlorinated biphenyls (PCB) as Aroclor 1254. Mortality was recorded and various tissues analyzed for PCB levels. Tissue concentrations of PCB increased in direct relation with the time of the experiment and with the survival period of

Expression of Biphenyl Synthase Genes and Formation of Phytoalexin Compounds in Three Fire Blight-Infected Pyrus communis Cultivars.

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Ingia / Ingia

Pear (Pyrus communis) is an economically important fruit crop. Drops in yield and even losses of whole plantations are caused by diseases, most importantly fire blight which is triggered by the bacterial pathogen Erwinia amylovora. In response to the infection, biphenyls and dibenzofurans are formed

Effects of co-exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin and polychlorinated biphenyls on nonalcoholic fatty liver disease in mice.

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Ingia / Ingia

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and polychlorinated biphenyls (PCBs) are persistent organic pollutants which coexist in environment, and human are co-exposed to these chemicals. Our present study was aimed to investigate the possible enhanced nonalcoholic fatty liver disease (NAFLD) in

Polychlorinated biphenyl 153 is a diet-dependent obesogen that worsens nonalcoholic fatty liver disease in male C57BL6/J mice.

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Ingia / Ingia

BACKGROUND Polychlorinated biphenyls (PCBs) are persistent environmental pollutants that are detectable in the serum of all American adults. Amongst PCB congeners, PCB 153 has the highest serum level. PCBs have been dose-dependently associated with obesity, metabolic syndrome and nonalcoholic fatty

Pathology of experimentally induced polybrominated biphenyl toxicosis in pregnant heifers.

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Ingia / Ingia

Toxicosis was induced in pregnant Holstein-Friesian heifers by giving polybrominated biphenyls a in gelatin capsules at the rate of 25 g/day. Initially, this dosage was approximately 67 mg/kg of body weight. Clinical signs were anorexia, excessive lacrimation and salivation, diarrhea, emaciation,

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