Organotropic formation and disappearace of 8-hydroxydeoxyguanosine in the kidney of Sprague-Dawley rats exposed to Adriamycin and KBrO3

Cho, Dae‐Hyun; Hong, Jin Tae; Chin, Kang; Cho, Tai Soon; Lee, Byung Mu

doi:10.1016/0304-3835(93)90235-2

Cited by 40 publications

(10 citation statements)

References 11 publications

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“…8-OHdG is thought to be a promutagenic lesion because this lesion induces G:C to T:A transversion unless repaired prior to replication (Cheng et al, 1992). It has been suggested -mation of 8-OHdG in the target organs of animals treated with free radical generating carcinogens (Cho et al, 1993). Oral administration of B [a]P to Sprague-Dawley rats increased hepatic 8-OHdG and decreased catalase and superoxide dismutase activities.…”

Section: Discussionmentioning

confidence: 99%

Protective role of metallothionein in benzo[a]pyrene-induced DNA damage

et al. 2009

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INTRODUCTION Benzo[a]pyrene (B[a]P) is one of the polycyclic aromatic hydrocarbons (PAH) referred to as a human carcinogen (IARC monographs, in preparation). B[a]P has beenshown to induce gene mutations, chromosomal aberrations and other types of genotoxic effects in in vitro and in vivo. Most humans are more or less constantly exposed to B[a]P. As a product of incomplete combustion, B[a]P is present in tobacco smoke, diesel engine exhaust, urban air, various types of processed foods, coal-tar, creosote, asphalt, and various occupational settings such as coal B[a]P is metabolized to 7,8-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE) by cytochrome P450 (P450 or CYP). BPDE is the ultimate carcinogenic form of B[a]P and binds to the exocyclic nitrogen of deoxyguanosine in DNA. BPDE-DNA adducts in target tissues were closely related to development of cancer in animals and humans (Culp and Beland, 1994). In addition, oxidative DNA damage also plays an important role in the process of B[a]P carcinogenesis, because B[a]P produces quinone derivatives which easily generate reactive oxygen species (ROS) and oxidatively damage DNA (Penning et al., 1996). As a result of hydroxyl radical interaction with DNA, many types of oxidized a]P administration, although that of wild-type mice was only slightly changed. Because cytochrome P450 (CYP) plays a major role in the process of B[a]P metabolic activation, we attempted to reveal the effect of MT on metabolic activation of B[a]P. Although CYP1A activities were elevated in the livers of MT-I/II null mice and wild-type mice treated with B[a]P, it was not different between both strains of mice. In addition, a]P treatment, whereas MT was not detected in livers of MT-I/II null mice with or without B[a]P treatment. These results demonstrate that MT acts as an endogenous defensive factor against B[a]P-induced DNA damage.

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Section: Discussionmentioning

confidence: 99%

Protective role of metallothionein in benzo[a]pyrene-induced DNA damage

et al. 2009

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“…115 Treatment of male B6C3F 1 mice with 75 mg/kg HQ, i.p., and of male SD rats with 250 mg/kg HQ, i.p., also did not result in increased 8-OHdG levels in bone marrow or in liver or kidney DNA, respectively. 111, 116 These studies indicate that HQ conversion to the semiquinone and BQ can potentially result in covalent adduction to both protein and DNA in vitro. In addition, formation of activated oxygen species via HQ oxidation can lead to increased 8-OHdG adduction in DNA in vitro.…”

Section: Macromolecular Binding and Redox Reactionsmentioning

confidence: 97%

The Toxicology of Hydroquinone — Relevance to Occupational and Environmental Exposure

DeCaprio¹

1999

Critical Reviews in Toxicology

178

128

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Hydroquinone (HQ) is a high-volume commodity chemical used as a reducing agent, antioxidant, polymerization inhibitor, and chemical intermediate. It is also used in over-the-counter (OTC) drugs as an ingredient in skin lighteners and is a natural ingredient in many plant-derived products, including vegetables, fruits, grains, coffee, tea, beer, and wine. While there are few reports of adverse health effects associated with the production and use of HQ, a great deal of research has been conducted with HQ because it is a metabolite of benzene. Physicochemical differences between HQ and benzene play a significant role in altering the pharmacokinetics of directly administered when compared with benzene-derived HQ. HQ is only weakly positive in in vivo chromosomal assays when expected human exposure routes are used. Chromosomal effects are increased significantly when parenteral or in vitro assays are used. In cancer bioassays, HQ has reproducibly produced renal adenomas in male F344 rats. The mechanism of tumorigenesis is unclear but probably involves a species-, strain-, and sex-specific interaction between renal tubule toxicity and an interaction with the chronic progressive nephropathy that is characteristic of aged male rats. Mouse liver tumors (adenomas) and mononuclear cell leukemia (female F344 rat) have also been reported following HQ exposure, but their significance is uncertain. Various tumor initiation/promotion assays with HQ have shown generally negative results. Epidemiological studies with HQ have demonstrated lower death rates and reduced cancer rates in production workers when compared with both general and employed referent populations. Parenteral administration of HQ is associated with changes in several hematopoietic and immunologic endpoints. This toxicity is more severe when combined with parenteral administration of phenol. It is likely that oxidation of HQ within the bone marrow compartment to the semiquinone or p-benzoquinone (BQ), followed by covalent macromolecular binding, is critical to these effects. Bone marrow and hematologic effects are generally not characteristic of HQ exposures in animal studies employing routes of exposure other than parenteral. Myelotoxicity is also not associated with human exposure to HQ. These differences are likely due to significant route-dependent toxicokinetic factors. Fetotoxicity (growth retardation) accompanies repeated administration of HQ at maternally toxic dose levels in animal studies. HQ exposure has not been associated with other reproductive and developmental effects using current USEPA test guidelines. The skin pigment lightening properties of HQ appear to be due to inhibition of melanocyte tyrosinase. Adverse effects associated with OTC use of HQ in FDA-regulated products have been limited to a small number of cases of exogenous ochronosis, although higher incidences of this syndrome have been reported with inappropriate use of unregulated OTC products containing higher HQ concentrations. The most serious human health effect related to HQ is p...

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“…8-Hydroxyl-2-deoxyguanosine (8-OHdG), a major byproduct of hydroxyl radical attack on DNA, is considered as a reliable biomarker for oxidative damage, because it can be quantitated with high sensitivity [6][7][8][9][10]. Besides, numerous studies provide evidence showing that 8-OHdG is also a key biomarker relevant to carcinogenesis [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Oxidative DNA damage is involved in cigarette smoke-induced lung injury in rats

Chen

Wang

Xing

et al. 2015

Environ Health Prev Med

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These findings indicate that long-term exposure to cigarette smoker increases ROS levels, decreases total antioxidant capacity, and interferes DNA repair capacity that eventually induces oxidative DNA damage, which appears to play an important role in cigarette smoke-induced lung injury in rats, and determination of 8-OHdG levels might be a useful method for monitoring oxidative damage in cigarette smokers.

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Organotropic formation and disappearace of 8-hydroxydeoxyguanosine in the kidney of Sprague-Dawley rats exposed to Adriamycin and KBrO3

Cited by 40 publications

References 11 publications

Protective role of metallothionein in benzo[a]pyrene-induced DNA damage

Protective role of metallothionein in benzo[a]pyrene-induced DNA damage

The Toxicology of Hydroquinone — Relevance to Occupational and Environmental Exposure

Oxidative DNA damage is involved in cigarette smoke-induced lung injury in rats

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