crotonaldehyde/nekroos

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Autophagy induced by low concentrations of crotonaldehyde promotes apoptosis and inhibits necrosis in human bronchial epithelial cells.

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Crotonaldehyde is a common environmental contaminant. Autophagy, apoptosis, and necrosis, were all respectively reported to be induced by crotonaldehyde. However, the relationships between programmed cell deaths, especially between autophagy and apoptosis, have not been elucidated. In the present

Long-term exposure to crotonaldehyde causes heart and kidney dysfunction through induction of inflammatory and oxidative damage in male Wistar rats.

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Crotonaldehyde is a ubiquitous hazardous pollutant, present in cigarette smoke and automobile exhaust and is endogenously generated by lipid peroxidation. Most of the current studies focus on its lung toxicity. However, there have been few investigations on the cardiac and renal toxicity caused by

[Effect of long-term crotonaldehyde exposure on heart damage in male rats].

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Objective: To observe the effect of long term crotonaldehyde exposure on heart damage in male rats, and to explore the possible mechanism of toxic action. Methods: 24 specific pathogen free healthy male wistar rats were randomly divided into 4 groups with 6 rats in each group. Rats were treated with

Acute exposure to crotonaldehyde induces dysfunction of immune system in male Wistar rats.

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Crotonaldehyde is a ubiquitous air pollutant in the environment. It is reported to be harmful to the biosystems in vivo and in vitro. The exposure to crotonaldehyde irritates the mucous membranes and induces edema, hyperemia, cell necrosis, inflammation, and acute respiratory distress syndrome in

Crotonaldehyde-exposed macrophages induce IL-8 release from airway epithelial cells through NF-κB and AP-1 pathways.

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Crotonaldehyde, a highly toxic α, β-unsaturated aldehyde, is a major component of cigarette smoke and a ubiquitous environmental pollutant. Crotonaldehyde exposure is known to have adverse effects on respiratory health, but the underlying mechanisms remain obscure. To examine the interaction between

Crotonaldehyde induces oxidative stress and caspase-dependent apoptosis in human bronchial epithelial cells.

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Crotonaldehyde is a widespread environmental pollutant and lipid peroxidation product. Crotonaldehyde is a risk factor for many diseases (e.g., chronic pulmonary inflammation). However, its toxicity and its mechanism of action have not been thoroughly investigated. The purpose of this study is to

[Study on lung injury induced by subchronic exposure to crotonaldehyde in male rats].

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Objective: To observe the lung injury of male rats induced by sub-chronic exposure to crotonaldehyde, and to explore the possible mechanism of injury. Methods: Forty SPF male Wistar rats were randomly divided into control group and 3 groups in each group, and each group received 0.0,

[Effect of crotonaldehyde long-term exposure induced kidney inflammatory and oxidative injury in male rats].

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Objective: To observe the effect of crotonaldehyde long-term exposure on kidney injury in male rats, and to explore the specific mechanism of toxic action. Methods: 32 specific pathogen free healthy adult male wistar rats were randomly divided into 4 groups with 8 rats in each group: high-,

Acrolein inhibits cytokine gene expression by alkylating cysteine and arginine residues in the NF-kappaB1 DNA binding domain.

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Cigarette smoke is a potent inhibitor of pulmonary T cell responses, resulting in decreased immune surveillance and an increased incidence of respiratory tract infections. The alpha,beta-unsaturated aldehydes in cigarette smoke (acrolein and crotonaldehyde) inhibited production of interleukin-2

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