Oxidative stress, apoptosis, and cell cycle arrest are induced in primary fetal alveolar type II epithelial cells exposed to fine particulate matter from cooking oil fumes

Abstract

Epidemiological studies demonstrate a linkage between morbidity and mortality and particulate matter (PM), particularly fine particulate matter (PM2.5) that can readily penetrate into the lungs and are therefore more likely to increase the incidence of respiratory and cardiovascular diseases. The present study investigated the compositions of cooking oil fume (COF)-derived PM2.5, which is the major source of indoor pollution in China. Furthermore, oxidative stress, cytotoxicity, apoptosis, and cell cycle arrest induced by COF-derived PM2.5 in primary fetal alveolar type II epithelial cells (AEC II cells) were also detected. N-acetyl-L-cysteine (NAC), a radical scavenger, was used to identify the role of oxidative stress in the abovementioned processes. Our results suggested that compositions of COF-derived PM2.5 are obviously different to PM2.5 derived from other sources, and COF-derived PM2.5 led to cell death, oxidative stress, apoptosis, and G0/G1 cell arrest in primary fetal AEC II cells. Furthermore, the results also showed that COF-derived PM2.5 induced apoptosis through the endoplasmic reticulum (ER) stress pathway, which is indicated by the increased expression of ER stress-related apoptotic markers, namely GRP78 and caspase-12. Besides, the induction of oxidative stress, cytotoxicity, apoptosis, and cell cycle arrest was reversed by pretreatment with NAC. These findings strongly suggested that COF-derived PM2.5-induced toxicity in primary fetal AEC II cells is mediated by increased oxidative stress, accompanied by ER stress which results in apoptosis.

Amelioration of the nephrotoxic effect of potassium dichromate by whey protein and/or nigella sativa oil in male albino rats

“…As the number of medicines, natural compounds, industrial elements and environmental pollutants that cause nephrotoxicity has increased, the importance of this disease will grow up till the scientists discover a natural solution that can be used as a protective and preventive tool against kidney damage (Liu et al, 2015). From these chemical and industrial nephrotoxic compounds is potassium dichromate, which is a potent oxidizing agent displaying a marked affinity, once reduced to trivalent chromium (Cr +3 ) by numerous cell metabolites, to .…”

Association between cooking oil fume exposure and lung cancer among Chinese nonsmoking women: a meta-analysis

“… 14 Cooking oil fume exposure increased oxidative stress and endoplasmic reticulum stress, which induced cytotoxicity and apoptosis in primary fetal alveolar epithelial cells (AEC) II cells. 15 Several studies have demonstrated that mutagens and carcinogens are released by fumes from heated cooking oils, using the Ames assay or SOS chromotest. 16 Biology experiments in human lung adenocarcinoma cells found that various mutagenic compounds were generated by cooking oil fume that lead to DNA damage and oxidative damage to cells.…”

Cooking Fumes and Relative Diseases

“…CONTACTS According to World Health Organization (WHO), there are approximately 1.6 million excess deaths annually among human-based combustion activities such as cooking and heating, which account for nearly 3 % of the global burden of diseases [27]. Due to the complex toxic compounds of CFs, CFs might caused lung toxicity, immune toxicity, hereditary toxicity, potential carcinogenicity and so on to organism.…”

“…Occupational exposure to CFs led to increased oxidative damage [4]. A complex mixture of particulates, metals, volatile organic compounds, polycyclic aromatic hydrocarbons (PAHs), benzene, quinines, and carbonyl compounds will produces during oil heating process, which were related to the formation of reactive oxygen species (ROS) and the induction of cellular events resulting in cell death [27]. Especially polycyclic aromatic hydrocarbons (PAHs) of CFs have carcinogenic properties on mucosal and endothelial lining of upper aero digestive tract [28].…”