Expression of Heme Oxygenase‐1 in the Lungs of Rats Exposed to Potassium Octatitanate Whiskers

Obata, Yasuko; Morimoto, Yasuo; Hirohashi, Masami; Ogami, Akira; Oyabu, Takako; Myojo, Toshihiko; Kawanami, Satoshi; Horie, Seichi; Nagatomo, Hiroko; Murakami, Masahirô; Tanaka, Isamu

doi:10.1539/joh.l10056

Cited by 6 publications

(2 citation statements)

References 20 publications

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“…It is not clear why CoPPIX did not result in HO-1 induction in hair cells or supporting cells in mouse utricles in vitro. The localization of HO-1 expression in macrophages observed herein is consistent with reports that HO-1 is expressed in macrophages of other organs, including liver and lung (Devey et al 2009;Obata et al 2011). Depletion of 75 % of the macrophages from utricular explants using LC abolished the protective effect of HO-1 induction (Fig.…”

Section: Discussionsupporting

confidence: 91%

Heat Shock Protein-Mediated Protection Against Cisplatin-Induced Hair Cell Death

Baker

Roy

Brandon

et al. 2014

JARO

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Cisplatin is a highly successful and widely used chemotherapy for the treatment of various solid malignancies in both adult and pediatric patients. Side effects of cisplatin treatment include nephrotoxicity and ototoxicity. Cisplatin ototoxicity results from damage to and death of cells in the inner ear, including sensory hair cells. We showed previously that heat shock inhibits cisplatin-induced hair cell death in whole-organ cultures of utricles from adult mice. Since heat shock protein 70 (HSP70) is the most upregulated HSP in response to heat shock, we investigated the role of HSP70 as a potential protectant against cisplatin-induced hair cell death. Our data using utricles from HSP70 −/− mice indicate that HSP70 is necessary for the protective effect of heat shock against cisplatin-induced hair cell death. In addition, constitutive expression of inducible HSP70 offered modest protection against cisplatin-induced hair cell death. We also examined a second heat-inducible protein, heme oxygenase-1 (HO-1, also called HSP32). HO-1 is an enzyme responsible for the catabolism of free heme. We previously showed that induction of HO-1 using cobalt protoporphyrin IX (CoPPIX) inhibits aminoglycoside-induced hair cell death. Here, we show that HO-1 also offers significant protection against cisplatin-induced hair cell death. HO-1 induction occurred primarily in resident macrophages, with no detectable expression in hair cells or supporting cells. Depletion of macrophages from utricles abolished the protective effect of HO-1 induction. Together, our data indicate that HSP induction protects against cisplatin-induced hair cell death, and they suggest that resident macrophages mediate the protective effect of HO-1 induction.

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Section: Discussionsupporting

confidence: 91%

Heat Shock Protein-Mediated Protection Against Cisplatin-Induced Hair Cell Death

Baker

Roy

Brandon

et al. 2014

JARO

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“…Other oxidant markers were also increased, such as the NOx concentration [ 22 ] and lipid peroxidation levels [ 22 ]. In response to ROS release, significant increases in the enzyme heme-oxygenase-1 (HO-1) are detected specifically in alveolar macrophages [ 121 ]. Antioxidant markers, such as glutathione peroxidase [ 17 ] and SOD activity [ 22 ], also increase significantly [ 22 ], in particular the mitochondrial Mn-SOD (at both mRNA and protein levels) [ 16 , 17 ].…”

Section: Biological Effects Of Micro- and Nanometric Crystalline Or A...mentioning

confidence: 99%

Pulmonary Toxicity of Silica Linked to Its Micro- or Nanometric Particle Size and Crystal Structure: A Review

et al. 2022

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Silicon dioxide (SiO2) is a mineral compound present in the Earth’s crust in two mineral forms: crystalline and amorphous. Based on epidemiological and/or biological evidence, the pulmonary effects of crystalline silica are considered well understood, with the development of silicosis, emphysema, chronic bronchitis, or chronic obstructive pulmonary disease. The structure and capacity to trigger oxidative stress are recognized as relevant determinants in crystalline silica’s toxicity. In contrast, natural amorphous silica was long considered nontoxic, and was often used as a negative control in experimental studies. However, as manufactured amorphous silica nanoparticles (or nanosilica or SiNP) are becoming widely used in industrial applications, these paradigms must now be reconsidered at the nanoscale (<100 nm). Indeed, recent experimental studies appear to point towards significant toxicity of manufactured amorphous silica nanoparticles similar to that of micrometric crystalline silica. In this article, we present an extensive review of the nontumoral pulmonary effects of silica based on in vitro and in vivo experimental studies. The findings of this review are presented both for micro- and nanoscale particles, but also based on the crystalline structure of the silica particles.

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Oxidative effects of lungs in Wistar rats caused by long-term exposure to four kinds of China representative chrysotile

Cui

Zha

et al. 2019

Environ Sci Pollut Res

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Expression of Heme Oxygenase‐1 in the Lungs of Rats Exposed to Potassium Octatitanate Whiskers

Cited by 6 publications

References 20 publications

Heat Shock Protein-Mediated Protection Against Cisplatin-Induced Hair Cell Death

Heat Shock Protein-Mediated Protection Against Cisplatin-Induced Hair Cell Death

Pulmonary Toxicity of Silica Linked to Its Micro- or Nanometric Particle Size and Crystal Structure: A Review

Oxidative effects of lungs in Wistar rats caused by long-term exposure to four kinds of China representative chrysotile

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