Pulmonary injury and antioxidant response in mice exposed to arsenate and hexavalent chromium and their combination

Tajima, Haruka; Yoshida, Toshinori; Ohnuma, Aya; Fukuyama, Tomoki; Hayashi, Kôichi; Yamaguchi, Satoru; Ohtsuka, Ryoichi; Sasaki, Junya; Tomita, Mariko; Kojima, Sayuri; Takahashi, Naofumi; Kashimoto, Yukiko; Kuwahara, Maki; Takeda, Makio; Kosaka, Toshio; Nakashima, Nobuaki; Harada, Takanori

doi:10.1016/j.tox.2009.10.032

Cited by 30 publications

(18 citation statements)

References 46 publications

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“…As with LMW-AST, changes in liver HMW-AST may refl ect lower gene expression in short-term exposure and then rise in the 45-day group as a consequence of suppression of chromium-induced oxidative stress by endogenous vitamin C biosynthesis, as reported by Mohan et al (18) and Hemmati et al (19). Lower HMW-AST activity in long-term (60-day) exposure may refl ect oxidative stress and the development of apoptosis (20) in soft tissues (21)(22)(23).…”

Section: Lmw-ast and Hmw-ast Isoenzymesmentioning

confidence: 99%

Liver Aspartate Transaminase Isoenzymes as Biomarkers of Chronic Exposure to Chromium(VI)

Najafi

Roustazadeh

Moshtaghie

et al. 2013

Archives of Industrial Hygiene and Toxicology

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Exposure to hexavalent chromium compounds is associated with the risk of lung cancer, dermatitis, gastrointestinal ulcers, and other tissue damages. The aim of this study was to compare liver isoenzyme and total serum activities of aspartate aminotransferase (AST) as cytotoxic biomarkers of acute and chronic cytotoxicity of Cr VI . We investigated the extent of cell damage caused by chromium(VI) in acute (2.5 mg kg -1 ) daily doses administered over fi ve days and chronic (0.25 mg kg -1 and 0.5 mg kg -1 ) daily doses administered over 15 to 60 days by measuring total AST in serum and low molecular weight AST (LMW-AST) and high molecular weight AST (HMW-AST) activities in thirty liver fractions. We also evaluated the kinetic properties and electrophoretic mobility of the LMW-and HMW-AST isoenzymes in liver subcellular fractions. Liver LMW-AST and total serum AST activities signifi cantly decreased after 15 days of exposure (P<0.05). With continued treatment, AST activity increased by 15.67 % (P<0.05). Interestingly, changes in serum AST activity were similar to changes in the liver LMW-AST isoenzyme. Our results confi rmed that total serum AST activity may serve as a reliable tissue biomarker for long-term exposures to Cr VI , but they also suggest that the LMW-AST isoenzyme could be even more sensitive.

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Section: Lmw-ast and Hmw-ast Isoenzymesmentioning

confidence: 99%

Liver Aspartate Transaminase Isoenzymes as Biomarkers of Chronic Exposure to Chromium(VI)

Najafi

Roustazadeh

Moshtaghie

et al. 2013

Archives of Industrial Hygiene and Toxicology

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“…A solvent, isopropyl alcohol for purification of DDAC, was not identified in the formulation. The mice (aged 8-12 weeks) were anesthetized with 50 mg/kg of pentobarbital and were subjected to intratracheal instillation of DDAC dissolved in phosphate-buffered saline (PBS) (150 µg/kg) into the lungs, as described previously (Ohnuma et al, 2010). Mice (n = 3-5 per group) were sacrificed on Days 1, 3, or 7 after administration.…”

Section: Animal Treatmentmentioning

confidence: 99%

“…Lavage of the lung was performed as previously described (Tajima et al, 2010), and bronchoalveolar lavage (BAL) supernatants were kept aside to assess protein concentration, lactate dehydrogenase (LDH) activity, and cytokine expression, using the methods described below. The BAL samples were pooled, and the total cell count was determined using the ADVIA120 Hematology System (Siemens Healthcare Diagnostics Inc., Illinois, U.S.A.).…”

Section: Tissue Preparation and Bronchoalveolar Lavagementioning

confidence: 99%

“…Recently, we found that a single instillation of DDAC causes pulmonary inflammation in mice 1 week after exposure, which is associated with the expression of several chemokines and their receptors; the inflammatory phase is accompanied or followed by a fibrotic response on Weeks 1 and 2 (Ohnuma et al, 2010). Accumulating evidence suggested that the development of bacteria resistant to DDAC becomes public health concern and raised the possibility that human exposed to DDAC increases risk for infection because of the direct toxic effect of DDAC on the respiratory system.…”

Section: Introductionmentioning

confidence: 99%

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Altered pulmonary defense system in lung injury induced by didecyldimethylammonium chloride in mice

Ohnuma¹,

Yoshida²,

Horiuchi³

et al. 2011

Inhalation Toxicology

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Didecyldimethylammonium chloride (DDAC), a representative dialkyl-quaternary ammonium compound (QAC), could contaminate working atmospheres when used in disinfectant operation and adversely affect human health. Furthermore, the development of bacteria resistant to DDAC might become public health concern. We postulated that DDAC instillation in the lungs alters pulmonary antioxidant and antimicrobial responses and increases susceptibility to systemic administration of a bacterial component lipopolysaccharide (LPS). Mice were intratracheally instilled with DDAC and sacrificed 1, 3, or 7 days after treatment. Pulmonary cytotoxicity in recovered bronchoalveolar lavage was evident on Days 1 and 7, and inflammatory cell influx and interleukin-6 expression peaked on Day 7, in association with altered antioxidant and antimicrobial responses, as demonstrated by measuring heme oxygenase-1, glutathione peroxidase 2, lactoferrin, and mouse β-defensin-2 and -3 mRNA in the lung samples. The impaired defense system tended to enhance the inflammatory reaction caused by a systemic administration of LPS; the effect was in association with increased expression of toll-like receptor-4 mRNA. The results suggest that DDAC alters pulmonary defense system, which may contribute to susceptibility to an exogenous infectious agent.

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“…Reduction of Cr(VI) to Cr(V) is required for the induction of DNA damage and mutations (Quievryn et al 2002). Genotoxic effects of chromium are predominantly represented by the formation of oxidative adducts and apurinic/apyrimidinic lesions, eventually resulting in DNA breaks (Balachandar et al 2010;Beveridge et al 2010;Figgitt et al 2010;Tajima et al 2010;Tsaousi et al 2010;Velma and Tchounwou 2010). It is notable that Cr also exhibits epigenetic effects in carcinogenesis, an inhibition of the nucleotide excision repair (NER) (Hodges and Chipman 2002).…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms of DNA Repair Genes and Lung Cancer in Chromium Exposure

Šarlinová

Majerová

Matáková

et al. 2014

Advances in Experimental Medicine and Biology

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Chromium is a well known carcinogen involved in the lung cancer development. Polymorphism of some of the DNA repair genes may be associated with elevated risk of cancerous transformation. In the present study, we investigated the polymorphisms of the following selected members of the base and nucleotide excision repair genes: XPC (Lys939Gln), XPD (Lys751Gln), XRCC1(Arg399Gln), and hOGG1(Ser326Ser), and the risk they present toward the development of lung cancer, with emphasis on the effect of chromium exposure. We analyzed 119 individuals; 50 patients exposed to chromium with diagnosed lung cancer and 69 healthy controls. Genotypes were determined by a PCR-RFLP method. We found a significantly increased risk of lung cancer development in XPD genotype Lys/Gln (OR=1.94; 95% CI=1.10-3.43; p=0.015) and in the gene combinations: XPD Lys/Gln+XPC Lys/Gln (OR=6.5; 95% CI=1.53-27.49; p=0.009) and XPD Lys/Gln+XPC Gln/Gln(OR=5.2; 95% CI=1.07-25.32; p=0.04). In conclusion, gene polymorphisms in the DNA repair genes may underscore the risk of lung cancer development in the chromium-exposed individuals.

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Pulmonary injury and antioxidant response in mice exposed to arsenate and hexavalent chromium and their combination

Cited by 30 publications

References 46 publications

Liver Aspartate Transaminase Isoenzymes as Biomarkers of Chronic Exposure to Chromium(VI)

Liver Aspartate Transaminase Isoenzymes as Biomarkers of Chronic Exposure to Chromium(VI)

Altered pulmonary defense system in lung injury induced by didecyldimethylammonium chloride in mice

Polymorphisms of DNA Repair Genes and Lung Cancer in Chromium Exposure

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