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001-es BibID:	BIBFORM047643
035-os BibID:	PMID:14599773
Első szerző:	Boldogh István
Cím:	Reduced DNA double strand breaks in chlorambucil resistant cells are related to high DNA-PKcs activity and low oxidative stress / Istvan Boldogh, Gargi Roy, Myung-Soog Lee, Attila Bacsi, Tapas K. Hazra, Kishor K. Bhakat, Gokul C. Das, Sankar Mitra
Dátum:	2003
ISSN:	0300-483X
Megjegyzések:	Modulation of DNA repair represents a strategy to overcome acquired drug resistance of cells to genotoxic chemotherapeuticagents, including nitrogen mustards (NM). These agents induce DNA inter-strand cross-links, which in turn produce doublestrand breaks (dsbs). These breaks are primarily repaired via the nonhomologous end-joining (NHEJ) pathway.ADNA-dependentprotein kinase (DNA-PK) complex plays an important role in NHEJ, and its increased level/activity is associated with acquireddrug resistance of human tumors. We show in this report that the DNA-PK complex has comparable levels and kinase activityof DNA-PK catalytic subunit (DNA-PKcs) in a nearly isogenic pair of drug-sensitive (A2780) and resistant (A2780/100) cells;however, treatment with chlorambucil (Cbl), a NM-type of drug, induced differential effects in these cells. The kinase activityof DNA-PKcs was increased up to 2 h after Cbl treatment in both cell types; however, it subsequently decreased only in sensitivecells, which is consistent with increased levels of DNA dsbs. The decreased kinase activity of DNA-PKcs was not due to a changein its amount or the levels ofKu70 andKu86, their subcellular distribution, cell cycle progression or caspase-mediated degradationof DNA-PK. In addition to DNA cross-links, Cbl treatment of cells causes a 2.2-fold increase in the level of reactive oxygenspecies (ROS) in both cell types. However, the ROS in A2780/100 cells were reduced to the basal level after 3?4 h, while sensitivecells continued to produce ROS and undergo apoptosis. Pre-treatment of A2780 cells with the glutathione (GSH) precursor,N-acetyl-l-cysteine prevented Cbl-induced increase in ROS, augmented the kinase activity of DNA-PKcs, decreased the levelsof DNA dsbs and increased cell survival. Depletion in GSH from A2780/100 cells by l-buthionine sulfoximine (BSO) resulted insustained production of ROS, loweredDNA-PKcs kinase activity, enhanced levels ofDNAdsbs, and increased cell killing by Cbl.We propose that oxidative stress decreases repair of DNA dsbs via lowering kinase activity of DNA-PKcs and that induction ofROS could be the basis for adjuvant therapies for sensitizing tumor cells to nitrogen mustards and other DNA cross-linking drugs.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Oxidative stress DNA-PK DNA double strand breaks
Megjelenés:	Toxicology. - 193 : 1-2 (2003), p. 137-152. -
További szerzők:	Roy, Gargi Myung-Soog, Lee Bácsi Attila (1967-) (immunológus) Hazra, Tapas K. Bhakat, Kishor K. Das, Gokul C. Mitra, Sankar
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM133187
035-os BibID:	(scopus)105019964666 (wos)001598503200001
Első szerző:	Ivanovics Bence
Cím:	Carbamate insecticide bendiocarb induces complex embryotoxic effects, including morphological, behavioral, transcriptional, and immunological alterations in zebrafish / Ivánovics Bence, Gazsi Gyöngyi, Varga Zoltán K., Staszny Ádám, Váradi Eszter, Varga Zsófia, Ács András, Tóth Márta, Domokos Apolka, Reining Márta, Vásárhelyi Erna, Póliska Szilárd, Kovács Róbert, Baska Ferenc, Filep Zoltán, Bácsi Attila, Kobolák Julianna, Urbányi Béla, Szabó István, Müller Tamás, Csenki-Bakos Zsolt, Czimmerer Zsolt
Dátum:	2026
ISSN:	1532-0456
Megjegyzések:	The emergence and spread of vector-borne diseases necessitate the increased use of insecticides, such as carbamates, raising concerns about their potential toxicological risks to non-target organisms, including humans. Bendiocarb, frequently applied in indoor spraying operations and detected in maternal and fetal circulation, warrants particular attention for its developmental toxicity. This study aimed to assess transcriptional and phenotypic effects of sublethal bendiocarb exposure at concentrations of 0.035, 0.2, 0.4, 0.75, and 1.5 mg/L, using zebrafish embryos, a vertebrate model for developmental toxicity testing. Our analyses revealed acetylcholinesterase inhibition-associated morphological and behavioral abnormalities, including reduced locomotor activity in response to both visual and tactile stimuli, as well as impaired non-associative learning. Transcriptomic analysis indicated activation of muscle, immune, and metabolic pathways, while neurodevelopmental, phototransduction, and cell proliferation processes were suppressed. Consistent with these molecular findings, structural damage was observed in the retina, skeletal muscle, and notochord. Furthermore, bendiocarb exposure disrupted neutrophil granulocyte distribution and impaired inflammatory responses. Altogether, our results provide new insights into the embryotoxic effects of bendiocarb, highlighting its potential to disrupt early vertebrate development. These findings provide mechanistic insight that may support more informed evaluations of potential public health risks associated with developmental exposure to carbamates.
Tárgyszavak:	Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Carbamate Developmental toxicity Behavioral alterations Immunotoxicity Zebrafish embryo
Megjelenés:	Comparative Biochemistry And Physiology C-Toxicology & Pharmacology. - 299 (2026), p. 1-18. -
További szerzők:	Gazsi Gyöngyi Varga Zoltán K. Staszny Ádám Váradi Eszter Varga Zsófia Ács András Tóth Márta (1986-) (biológus) Domokos Apolka Reining Márta Vásárhelyi Erna Póliska Szilárd (1978-) (biológus) Kovács Róbert Baska Ferenc Filep Zoltán Bácsi Attila (1967-) (immunológus) Kobolák Julianna Urbányi Béla (Gödöllő) Szabó István Müller Tamás (Gödöllő) Csenki-Bakos Zsolt Czimmerer Zsolt (1981-) (molekuláris biológus)
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