A comparative study of protein carbonylation and mitochondrial dysfunction using the neurotoxicants 1,3-dinitrobenzene, 3-nitropropionic acid, and 3-chloropropanediol

Steiner, Stephen R.; Milton, Evan C.; Philbert, Martin A.

doi:10.1016/j.neuro.2013.04.004

Cited by 17 publications

(11 citation statements)

References 42 publications

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“…It has been suspected that oxidative stress and the disturbance of cellular redox balance might play a role in 3-MCPD toxicity (Skamarauskas et al, 2007;Steiner et al, 2013). Intriguingly, a number of deregulated proteins are either engaged in the catalysis of redox reactions or themselves subject to functional posttranslational modification by redox signaling.…”

Section: Discussionmentioning

confidence: 99%

Proteomic analysis of 3-MCPD and 3-MCPD dipalmitate toxicity in rat testis

Sawada

Oberemm

Buhrke

et al. 2015

Food and Chemical Toxicology

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Section: Discussionmentioning

confidence: 99%

Proteomic analysis of 3-MCPD and 3-MCPD dipalmitate toxicity in rat testis

Sawada

Oberemm

Buhrke

et al. 2015

Food and Chemical Toxicology

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“…It has been suggested that the toxicity of 3-MCPD is, at least in part, mediated by disturbance of the cellular redox state and oxidative stress phenomena (Skamarauskas et al 2007;Steiner et al 2013). The significant deregulation of the glutathione metabolism-related proteins Gstp1, Gss and Gpx4 (Table 1 and Table S1) seemed to support this hypothesis.…”

Section: Alterations In Gstp1 Expression and Involvement Of Nrf2mentioning

confidence: 91%

“…Due to the possible involvement of oxidative stress in 3-MCPD-caused toxicity (Skamarauskas et al 2007;Steiner et al 2013) and the effects of 3-MCPD on several enzymes engaged in glutathione metabolism, we analyzed whether Nrf2, a redox-sensitive transcription factor that plays a central role in protection against oxidant-and xenobiotic-induced cellular stress in kidney and other organs (Harvey et al 2009;Kim and Vaziri 2010;Li and Kong 2009), might be activated in rat kidney upon 3-MCPD treatment. It is widely accepted that Nrf2 activation confers protection against tissue injury (Kim and Vaziri 2010), especially during ischemic and nephrotoxic acute kidney injury (Liu et al 2009).…”

Section: Namesmentioning

confidence: 99%

Proteomic analysis of 3-MCPD and 3-MCPD dipalmitate-induced toxicity in rat kidney

et al. 2015

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3-Chloropropane-1,2-diol (3-MCPD) and its fatty acid esters are formed during thermal treatment of fat-containing foodstuff in the presence of salt. Toxicological studies indicate a carcinogenic potential of 3-MCPD, pointing to the kidney as the main target organ. It is assumed that the toxicological property of 3-MCPD esters is constituted by the release of 3-MCPD during digestion. In a repeated-dose 28-day oral toxicity study using Wistar rats, animals were treated with equimolar doses of either 3-MCPD (10 mg/kg body weight) or 3-MCPD dipalmitate (53 mg/kg body weight). A lower dose of 3-MCPD dipalmitate (13.3 mg/kg body weight) was also applied. No histopathologically visible toxicity was observed in the study. To address molecular mechanisms leading to toxicity of 3-MCPD and its esters, kidney samples were analyzed by a comparative, two-dimensional gel electrophoresis/mass spectrometry proteomic approach. After either 3-MCPD or 3-MCPD dipalmitate treatment, alterations in proteins related to various metabolic pathways, including carbohydrate, amino acid, and fatty acid metabolism, were detected. These findings confirm and complement previous data on the inhibition of glucose metabolism by 3-MCPD. Altogether, broad overlap of 3-MCPD- and 3-MCPD dipalmitate-induced proteomic changes was observed. Further analyses revealed that the observed induction of glutathione S-transferase pi 1 (Gstp1) occurred at the transcriptional level and was not related to nuclear factor (erythroid-derived 2)-like 2 activation. Overall, the results indicate common mechanisms of toxicity for 3-MCPD and its dipalmitate ester. Furthermore, data suggest Gstp1 as a sensitive marker for early 3-MCPD-induced effects in rat kidney.

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“…Rcn3 KO lungs at both E15. 5 Glycogen was normally accumulated in immature ATII cells and converted into phospholipids to produce lamellar bodies during ATII cell maturation (10)(11)(12). Lamellar body membrane protein ATP-binding cassette (ABC) A3 (ABCA3, a lipid transporter protein) is required for lamellar body formation in ATII cells (15).…”

Section: Rcn3 Is Essential For Functional Maturation Of Atii Cellsmentioning

confidence: 99%

Neonatal Respiratory Failure with Retarded Perinatal Lung Maturation in Mice Caused by Reticulocalbin 3 Disruption

Jin

Ren

et al. 2016

Am J Respir Cell Mol Biol

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Reticulocalbin 3 (Rcn3) is an endoplasmic reticulum lumen protein localized to the secretory pathway. As a Ca2t-binding protein of 45 kDa (Cab45)/Rcn/ER Ca2t-binding protein of 55 kDa (ERC45)/calumenin (CREC) family member, Rcn3 is reported to function as a chaperone protein involved in protein synthesis and secretion; however, the biological role of Rcn3 is largely unknown. The results presented here, for the first time, depict an indispensable physiological role of Rcn3 in perinatal lung maturation by using an Rcn3 gene knockout mouse model. These mutant mice die immediately at birth owing to atelectasis-induced neonatal respiratory distress, although these embryos are produced with grossly normal development. This respiratory distress results from a failure of functional maturation of alveolar epithelial type II cells during alveogenesis. This immaturity of type II cells is associated with a dramatic reduction in surfactant protein A and D, a disruption in surfactant phospholipid homeostasis, and a disorder in lamellar body. In vitro studies further show that Rcn3 deficiency blunts the secretion of surfactant proteins and phospholipids from lung epithelial cells, suggesting a decrease in availability of surfactants for their surface activity. Collectively, these observations indicate an essential role of Rcn3 in perinatal lung maturation and neonatal respiratory adaptation as well as shed additional light on the mechanism of neonatal respiratory distress syndrome development.

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A comparative study of protein carbonylation and mitochondrial dysfunction using the neurotoxicants 1,3-dinitrobenzene, 3-nitropropionic acid, and 3-chloropropanediol

Cited by 17 publications

References 42 publications

Proteomic analysis of 3-MCPD and 3-MCPD dipalmitate toxicity in rat testis

Proteomic analysis of 3-MCPD and 3-MCPD dipalmitate toxicity in rat testis

Proteomic analysis of 3-MCPD and 3-MCPD dipalmitate-induced toxicity in rat kidney

Neonatal Respiratory Failure with Retarded Perinatal Lung Maturation in Mice Caused by Reticulocalbin 3 Disruption

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