J
Johan Högberg
Researcher at National Institute of Occupational Health
Publications - 15
Citations - 477
Johan Högberg is an academic researcher from National Institute of Occupational Health. The author has contributed to research in topics: Glutathione & Hepatocyte. The author has an hindex of 10, co-authored 15 publications receiving 472 citations.
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Journal ArticleDOI
Genetic polymorphism of cytochrome P4502E1 in a Swedish population : relationship to incidence of lung cancer
I. Persson,Inger Johansson,Helene Bergung,Marja-Liisa Dahl,Janeric Seidegård,Ragnar Rylander,Agneta Rannug,Johan Högberg,Magnus Ingelman Sundberg +8 more
TL;DR: It is concluded that major interethnic differences exist in the genetic polymorphism of CYP2E1 and that people carrying the mutated allele (c2) among the lung cancer patients as compared to controls might be at lower risk for developing lung cancer.
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Studies of the role of DNA fragmentation in selenium toxicity.
TL;DR: Data from isolated hepatocyte model systems indicate a modulating role for DNA damage in selenite cytotoxicity mediated by poly(ADP-ribose)polymerase and suggest that cell death resulted from interactions between several events that may deplete energy supplies.
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Recovery of malondialdehyde in urine as a 2,4-dinitrophenylhydrazine derivative analyzed with high-performance liquid chromatography.
TL;DR: Monitoring MDA excretion in urine can give useful information about lipid peroxidation in vivo, and the peak urinary concentration approached the expected plasma concentration and reproducible recovery data were obtained, suggesting that MDA was passively excreted in a reasonably stable form.
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The role of GSH depletion and toxicity in hydroquinone-induced development of enzyme-altered foci.
TL;DR: It is concluded that the foci data provide no evidence for an involvement of redox cycles in hydroquinone-induced development of enzyme-altered foci, and in vitro data indicate a mechanism by which GSH depletion and toxicity may induce this effect.
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GST-P-positive hepatocytes isolated from rats bearing enzyme-altered foci show no signs of p53 protein induction and replicate even when their DNA contains strand breaks
Ulla Stenius,Johan Högberg +1 more
TL;DR: It is suggested that GST-P-positive cells lack functional p53 protein and that this permits cells with damaged DNA to replicate and is eliminated by p53 antisense oligonucleotides.