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  • 1
    Language: German
    Source: Münchener DigitalisierungsZentrum (Bayerische Staatsbibliothek)
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  • 2
    Language: German
    Subject(s): Bomhard, Eduard Von ; Bomhard ; Familie, Franken ; 1809-1886 ; Genealogie
    Source: Münchener DigitalisierungsZentrum (Bayerische Staatsbibliothek)
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  • 3
    Language: English
    Source: Walter de Gruyter GmbH
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  • 4
    Language: English
    In: Archives of Toxicology, 2013, Vol.87(7), pp.1201-1218
    Description: Classification for fertility is based on two conditions, namely on evidence of an adverse effect on sexual function and fertility and that the effect is not secondary to other toxic effects. To decide on an adverse effect is a relatively simple day-to-day decision in toxicology but whether this effect is secondary often leads to serious controversy. As the seminiferous epithelium operates on the verge of hypoxia, oxygen deficit can lead to secondary impairment of testicular function. This is well known from healthy mountaineers exposing themselves to high altitude. They have reduced blood oxygen content that goes in parallel with impairment of testicular function and this effect remains for some time in spite of a compensatory polycythaemia. Similar findings are described for experimental animals exposed to hypobaric oxygen/high altitude. In addition, testicular function is affected in severe diseases in humans associated with systemic oxygen deficit like chronic obstructive pulmonary disease, sickle cell disease or beta-thalassaemia as well as in transgenic animals simulating haemolytic anaemia or sickle cell disease. The problem of insufficient oxygen supply as the underlying cause for testicular impairment has received relatively little attention in toxicology, mainly because blood oxygen content is generally not measured in these animal experiments. The difficulties associated with the decision whether testicular toxicity is primary or secondary to hypoxia are exemplified by the results of inhalation studies with nickel subsulphide and gallium arsenide (GaAs). Both of these particulate substances lead to severe lung toxicity that might impair oxygen uptake, but testicular toxicity is only observed with GaAs. This may first be explained by different effects on the blood: nickel subsulphide inhalation leads to a compensatory erythropoiesis that may mitigate pulmonary lack of oxygen uptake. In contrast, GaAs exposure is associated with microcytic haemolytic anaemia thereby aggravating any possible oxygen undersupply. Furthermore, the predominant pulmonary effect caused by GaAs (but not by nickel subsulphide) is alveolar proteinosis. Pulmonary alveolar proteinosis is also known as a severe disease in humans associated with hypoxaemia. Therefore, we conclude that the testicular effects observed after GaAs are secondary to hypoxaemia caused by the combination of pulmonary proteinosis and haemolytic anaemia. This publication tries to raise awareness to the severe consequences of hypoxaemia on testicular function that may already be caused by reduced oxygen pressure at high altitude without any chemical exposure.
    Subject(s): Hypoxia ; Lung disease ; Blood disease ; Lung toxicity ; Blood toxicity ; Testicular toxicity ; Male fertility ; Gallium arsenide ; Nickel subsulphide
    ISSN: 0340-5761
    E-ISSN: 1432-0738
    Source: Springer Science & Business Media B.V.
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  • 5
    Language: English
    In: Archives of toxicology, July 2013, Vol.87(7), pp.1201-18
    Description: Classification for fertility is based on two conditions, namely on evidence of an adverse effect on sexual function and fertility and that the effect is not secondary to other toxic effects. To decide on an adverse effect is a relatively simple day-to-day decision in toxicology but whether this effect is secondary often leads to serious controversy. As the seminiferous epithelium operates on the verge of hypoxia, oxygen deficit can lead to secondary impairment of testicular function. This is well known from healthy mountaineers exposing themselves to high altitude. They have reduced blood oxygen content that goes in parallel with impairment of testicular function and this effect remains for some time in spite of a compensatory polycythaemia. Similar findings are described for experimental animals exposed to hypobaric oxygen/high altitude. In addition, testicular function is affected in severe diseases in humans associated with systemic oxygen deficit like chronic obstructive pulmonary disease,...
    Subject(s): Fertility -- Drug Effects ; Hypoxia -- Chemically Induced ; Testicular Diseases -- Chemically Induced ; Testis -- Drug Effects
    ISSN: 0340-5761
    E-ISSN: 1432-0738
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  • 6
    Language: English
    In: Archives of Toxicology, 2003, Vol.77(5), pp.291-297
    Description: To clarify the question of clastogenicity of aniline in rats two studies were performed: a bone marrow micronucleus test and a bone marrow metaphase test. In the micronucleus test aniline (as aniline hydrochloride) was administered to groups of seven male PVG rats at single oral doses of 0, 300, 400, or 500 mg/kg body weight. Bone marrow was obtained 24 and 48 h after oral treatment. Smears of bone marrow were stained with acridine orange and erythrocytes were examined for the presence of micronuclei. Animals receiving cyclophosphamide (1×7.5 mg/kg) served as positive controls. Clinical signs observed in animals dosed at 300 mg/kg and above included cyanosis, light brown coloured urine and cold to touch. Small, but statistically significant and dose-related increases in the incidence of micronulei over the vehicle control values were observed at the 24-h sampling time only. Cyclophosphamide induced a significant and comparably much higher increase in micronuclei than aniline. In the bone marrow metaphase test aniline (as aniline hydrochloride) was administered to groups of seven male PVG rats at single oral dose levels of 0, 300, 400, or 500 mg/kg body weight. Bone marrow was sampled 18 and 30 h after dosing. A group treated with cyclophosphamide (1×40 mg/kg) served as positive control. A small increase in the percentage of aberrant cells above solvent control values was recorded in one rat at 400 mg/kg and four rats at 500 mg/kg at the 18-h sampling time only. The positive control cyclophosphamide induced a much higher rate of aberrant cells in all animals. Several lines of evidences are presented against a causal relationship between the clastogenic activity in male PVG rats at 400 and 500 mg/kg and the carcinogenicity in the spleen of Fischer 344 rats starting at 30 mg/kg in males. Among these are the dose-response relationship of the tumour incidence, the close correlation between degree of spleen damage and tumour induction, the lack of carcinogenic effects in mice even at higher dose levels, or in rats at dose levels inducing only slight haematotoxicity and spleen toxicity, and the available data on the mode of action of other chemicals inducing spleen tumours.
    Subject(s): Genotoxicity Aniline hydrochloride Haematotoxicity Oxidative stress Non-genotoxic carcinogenicity
    ISSN: 0340-5761
    E-ISSN: 1432-0738
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  • 7
    Language: English
    In: Kidney International, February 1999, Vol.55(2), pp.529-545
    Description: Direct lysosomal uptake of α2-microglobulin contributes to chemically induced nephropathy. An abnormal accumulation of α2-microglobulin (α2μ) in kidney lysosomes of male rats has been described in the nephropathy resulting from exposure to a variety of chemicals. The increment in lysosomal levels of α2μ cannot be explained by a decrease in its proteolytic susceptibility. Because a portion of α2μ resides in the cytosol of kidney cells, we decided to analyze whether this cytosolic form also contributes to the abnormal lysosomal accumulation of α2μ after exposure to chemicals. Intact kidney lysosomes were isolated from untreated or 2,2,4-trimethylpentane (TMP) treated rats, and their ability to take up α2μ was compared. α2μ can be directly transported into isolated lysosomes in the presence of the heat shock cognate protein of 73kDa (hsc73). α2μ specifically binds to a lysosomal membrane glycoprotein of 96kDa, previously identified...
    Subject(s): Hyaline Droplet Nephropathy ; Lysosomes ; Heat Shock Protein ; Protein Degradation ; Cathepsin ; Membrane Transport ; Hyaline Droplet Nephropathy ; Lysosomes ; Heat Shock Protein ; Protein Degradation ; Cathepsin ; Membrane Transport ; Medicine
    ISSN: 0085-2538
    E-ISSN: 1523-1755
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  • 8
    Language: English
    In: Critical Reviews in Toxicology, 01 January 2005, Vol.35(10), pp.783-835
    Description: Aniline (in the form of its hydrochloride) has been shown to induce a rather rare spectrum of tumors in the spleen of Fischer 344 rats. The dose levels necessary for this carcinogenic activity were in a range where also massive effects on the...
    Subject(s): Aniline ; Rats ; Spleen Tumors ; Primary Genetic Activity ; Clastogenic Activity ; Mouse Lymphoma Tests ; Pharmacy, Therapeutics, & Pharmacology ; Public Health
    ISSN: 1040-8444
    E-ISSN: 1547-6898
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  • 9
    Language: English
    In: Toxicology, 1998, Vol.131(2), pp.73-91
    Description: Time course of enzyme induction was measured in Fischer344 rats treated daily at 150 and 600 mg 1,4-dichlorobenzene (1,4-DCB)/kg p.o. up to 28 days. The monoxygenases 7-ethoxycoumarin O-deethylase (ECOD), 7-ethoxyresorufin O-deethylase (EROD) and aldrin epoxidase (ALD) as well as the phase II enzymes; epoxide hydrolase (EH), glutathione S-transferase (GS-T) and glucuronyl transferase (GLU-T) were dose-dependently induced in the liver of males and females. A pronounced induction in the kidneys was measured at 600 mg/kg only for ECOD. After single oral administration of 100 and 1000 mg/kg bw and feeding of 100 and 1000 ppm (corresponding to ≈10 and 100 mg/kg bw) to male Wistar rats for 28 days, the time course of 1,4-DCB and 2,5-DCP concentrations was investigated in plasma, adipose, hepatic and renal tissue. In addition, total urinary excretion of 2,5-DCP was determined. After single application, 1,4-DCB and 2,5-DCP were rapidly eliminated from the plasma and tissues, 40–60%...
    Subject(s): 1,4-Dichlorobenzene ; Enzyme Induction ; Liver ; Kidneys ; Absorption ; Distribution ; 2,5-Dichlorophenol ; 1,4-Dichlorobenzene ; Enzyme Induction ; Liver ; Kidneys ; Absorption ; Distribution ; 2,5-Dichlorophenol ; ALD, Aldrin Epoxidase ; Cet, Central European Time ; Cyp, Cytochrome P 450 ; 1,4-Dcb, 1,4-Dichlorobenzene ; 2,5-Dcp, 2,5-Dichlorophenol ; Ecod, 7-Ethoxycoumarin O-Deethylase
    ISSN: 0300-483X
    E-ISSN: 1879-3185
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  • 10
    Language: English
    In: Mut.Res.-Genetic Toxicology and Environmental Mutagenesis, 2000, Vol.470(2), pp.161-167
    Description: The genotoxic potential of 1,4-dichlorobenzene (1,4-DCB) has been extensively evaluated in vitro and in vivo. The majority of the studies demonstrated the absence of a genotoxic potential for 1,4-DCB. At variance are a bone marrow micronucleus test (MNT) after intraperitoneal (i.p.) treatment of NMRI mice [Mohtashamipur et al., Mutagenesis 2 (1987) 111–113] and a gene mutation assay on mouse lymphoma cells [McGregor et al., Environ. Mol. Mutagen. 12 (1988) 85–145]. Therefore, we investigated 1,4-DCB and its main metabolite 2,5-dichlorophenol (2,5-DCP) for both endpoints. In an MNT, male and female NMRI mice were treated orally with single doses of 2500 mg/kg 1,4-DCB and 1500 mg/kg 2,5-DCP, respectively. Smears were prepared 24, 48 and 72 h thereafter. No induction of micronuclei was detected for both compounds. Also under the conditions of Mohtashamipur et al. (1987), intraperitoneal treatments of male and female mice with 2 × 177.5 and 2 × 355 mg/kg 1,4-DCB failed...
    Subject(s): Mouse Bone Marrow Micronucleus Test ; Hprt Gene Mutation Assay ; Mutation Frequency ; 1,4-Dichlorobenzene ; 2,5-Dichlorophenol ; Mouse Bone Marrow Micronucleus Test ; Hprt Gene Mutation Assay ; Mutation Frequency ; 1,4-Dichlorobenzene ; 2,5-Dichlorophenol ; Biology ; Public Health
    ISSN: 1383-5718
    E-ISSN: 1879-3592
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