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benzene/jagung

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Influence of multiwalled carbon nanotubes with outer diameters > 50 nm (MW) and a surfactant sodium dodecyl benzene sulfonate (SDBS) on bioaccumulation and translocation of pyrene and 1-methylpyrene (1-CH3-pyrene) in maize seedlings in single-(F1) and bi-(F2) compound systems was investigated.
A 7-day-exposure time experiment was designed to investigate the phytotoxicity of chlorobenzenes (CBs) on Zea mays seedlings, focusing on the growth and generation of oxidative stress. Significant growth inhibition (based on biomass gain) was observed for exposure to monochlorobenzene (MCB),

Promoting effects of 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene in mouse hepatocarcinogenesis.

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The effects of phenobarbital (PB) and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) on liver hyperplasia, induction of microsomal enzyme activities, and two-stage hepatocarcinogenesis were evaluated in B6C3F1 female mice. For 4 weeks four groups of mice received PB (500 p.p.m. in the drinking

Detection of nitrated benzene metabolites in bone marrow of B6C3F1 mice treated with benzene.

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Benzene, a constituent of cigarette smoke, is a human leukemogen and induces bone marrow toxicity. The mechanism of benzene-induced toxicity is not well-established. We hypothesized that relatively high levels of nitric oxide formed in bone marrow can react with oxygen and/or superoxide anion that

Benzene increases protein-bound 3-nitrotyrosine in bone marrow of B6C3F1 mice.

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Benzene, an environmental pollutant, is myelotoxic and leukemogenic in humans. The molecular mechanisms that can account for its biological effects have not been fully elucidated. We hypothesize that one of the underlying mechanism involves nitration of proteins by peroxynitrite and/or by bone
OBJECTIVE To investigate the effects of benzene poisoning on the expression of multidrug resistance 1 (MDR1) gene and P-glycoprotein (P-gp) in the bone marrow mononuclear cells (BMMNCs) of C57BL/6 mice. METHODS C57BL/6 mice were randomly divided into control group (n = 24), low-dose group (n = 24),

Modifications in the metabolic pathways of benzene in streptozotocin-induced diabetic rat.

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Benzene is a ubiquitous environmental pollutant primarily metabolized by a cytochrome P-450 (CYP-450) isoenzyme, CYP-450 IIE1. A consistent induction of CYP450 IIE1 has been observed in both rat and human affected by diabetes mellitus. The aim of this study was to evaluate whether streptozotocin
Diazoaminobenzene (DAAB), a manufacturing intermediate metabolized primarily to the known carcinogens benzene and aniline, has been identified as an impurity in a number of dyes and coloring agents that are components of cosmetics, food products, and pharmaceuticals. Several structural analogs of
Benzene is a well-known environmental pollutant that can induce hematotoxicity, aplastic anemia, acute myelogenous leukemia, and lymphoma. However, although benzene metabolites are known to induce oxidative stress and disrupt the cell cycle, the mechanism underlying lympho/leukemogenicity is not

Learning impairments following postnatal exposure to benzene.

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Two groups of male hooded rats of the Sprague-Dawley strain were administered 550 mg/kg of benzene in corn oil or pure corn oil on Days 9, 11, and 13 postpartum. When tested on problems of the Hebb-Williams closed-field maze-learning task, the rats previously exposed to benzene manifest
Benzene (C6H6) is one of the most commonly used industrial chemicals causing environmental pollution. This study aimed to examine the effect of benzene and its metabolite hydroquinone on glucose regulating organs, liver and pancreas, and to reveal the involved toxic mechanisms, in rats. In the in

Postnatal exposure to benzene alters the neurobehavioral functioning of rats when tested during adulthood.

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Male and female rats of the Fischer Strain were dosed with 550 mg/kg of benzene or corn oil vehicle on Days 9, 11 and 13 postpartum. The spontaneous motor activity of benzene exposed rats (males and females) was found to be elevated when tested at 100-130 days of age. When challenged with various

Transplacental benzene exposure increases tumor incidence in mouse offspring: possible role of fetal benzene metabolism.

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Childhood cancer is the leading cause of disease-related death in children aged 1-14 years in Canada and the USA and it has been hypothesized that transplacental exposure to environmental carcinogens such as benzene may contribute to the etiology of these cancers. Our objectives were to determine if

NTP Toxicology and Carcinogenesis Studies of Benzene (CAS No. 71-43-2) in F344/N Rats and B6C3F1 Mice (Gavage Studies).

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Benzene ranks 16th in production volume for chemicals produced in the United States, with approximately 9.9 billion pounds being produced in 1984, 9.1 billion pounds in 1983, and 7.8 billion pounds in 1982. This simplest aromatic chemical in used in the synthesis of styrene (polystyrene plastics and
Benzene is used primarily as a solvent in the chemical and pharmaceutical industries, as a starting material and intermediate in the synthesis of numerous chemicals, and in gasoline. The major United States source of benzene is petroleum. Benzene has been previously evaluated in 2-year
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