SO2 Inhalation Contributes to the Development and Progression of Ischemic Stroke in the Brain

Abstract

Epidemiological literatures show an association between air pollution and ischemic stroke, and effective pollutants may include SO(2), NO(x), O(3), CO, and particulates. However, existing experimental studies lack evidence as to the presence of effects for SO(2), which has been the focus in developing countries with increasing use of coal as the main resource. In the present study, we treated Wistar rats with SO(2) at various concentrations and determined endothelin-1 (ET-1), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and intercellular adhesion molecule 1 (ICAM-1) messenger RNA (mRNA) and protein expression in the cortex. The results show that SO(2) elevated the levels of ET-1, iNOS, COX-2, and ICAM-1 mRNA and protein in a concentration-dependent manner. Then, we set up rat model of ischemic stroke using middle cerebral artery occlusion (MCAO) and further treated the model rats with filtered air and lower concentration SO(2) for the same period. As expected, elevated expression of ET-1, iNOS, COX-2, and ICAM-1 occurred in the cortex of MCAO model rats exposed to filtered air, followed by increased activation of caspase-3 and cerebral infarct volume. Interestingly, SO(2) inhalation after MCAO significantly amplified above effects. It implies that SO(2) inhalation caused brain injuries similar to that of cerebral ischemia, and its exposure in atmospheric environment contributed to the development and progression of ischemic stroke.

A near-infrared fluorescent probe for rapid, colorimetric and ratiometric detection of bisulfite in food, serum, and living cells

“…On the other hand, sulfur dioxide (SO 2 ) is one of the most widely distributed air pollutants and is well known to have significant impacts upon human health [4]. Studies have shown that frequent exposure to SO 2 not only induces many respiratory responses [5], but is also linked to lung and brain cancer, cardiovascular disease, and neurological disorders [6]. Since SO 2 can be easily hydrated to sulfurous acid once inhaled and subsequently forms equilibrium of its derivatives bisulfite and sulfite as its main form in aqueous media, the toxicity of SO 2 is considered mainly by these two anions [7].…”

In vivo screening to determine neurological hazards of nitrogen dioxide (NO2) using Wistar rats

“…In the study, rats (n = 6/group) were exposed for 6 h/d for 7 d to fresh air, 5, 10 or 20 mg/m 3 NO 2 using protocol of dynamic inhalation based on our previous studies [25,26]. During exposure period, the four groups of rats were placed in 1 m 3 exposure chambers simultaneously.…”

The selective mGluR5 agonist CHPG attenuates SO2-induced oxidative stress and inflammation through TSG-6/NF-κB pathway in BV2 microglial cells

“…Inhaling SO2 is associated with increased respiratory symptoms and responses, and recent studies also imply that SO2 exposure is linked with many neurological disorders, such as stroke and brain cancer (Kampa and Castanas, 2008;Sang et al, 2010). SO2 derivatives were shown to cause apoptotic neuronal death through regulating several apoptosis-related genes, such as p53, bax, bcl-2 and c-jun .…”