Impact of commercial cigarette smoke condensate on brain tissue co-cultured with astrocytes and blood–brain barrier endothelial cells

Abstract

The purpose of the current study was to investigate the effect of two commercial cigarette smoke condensates (CCSC) on oxidative stress and cell cytotoxicity in human brain (T98G) or astrocytes (U-373 MG) in the presence of human brain microvascular endothelial cells (HBMEC). Cell viability of mono-culture of T98G or U-373 MG was markedly decreased in a concentration-dependent manner, and T98G was more susceptible than U-373 MG to CCSC exposure. Cytotoxicity was less prominent when T98G was co-cultured with HBMEC than when T98G was co-cultured with U-373 MG. Significant reduction in trans-epithelial electric resistance (TEER), a biomarker of cellular integrity was noted in HBMEC co-cultured with T98G (HBMEC-T98G co-culture) and U-373 MG co-cultured with T98G (U-373 MG-T98G co-culture) after 24 or 48 hr CCSC exposure, respectively. TEER value of U-373 MG co-cultured with T98G (79-84%) was higher than HBMEC co-cultured with T98G (62-63%) within 120-hr incubation with CCSC. Reactive oxygen species (ROS) generated by CCSC in mono-culture of T98G and U-373 MG reached highest levels at 4 and 16 mg/ml, respectively. ROS production by T98G fell when co-cultured with HBMEC or U-373MG. These findings suggest that adverse consequences of CCSC treatment on brain cells may be protected by blood-brain barrier or astrocytes, but with chronic exposure toxicity may be worsened due to destruction of cellular integrity.

Catechins Controlled Bioavailability of Benzo[a]pyrene (B[α]P) from the Gastrointestinal Tract to the Brain towards Reducing Brain Toxicity Using the In Vitro Bio-Mimic System Coupled with Sequential Co-Cultures

“…When IC 50 of B[α]P was compared between the HBMECs and the HepG2, the HBMECs (7.7 μM) were slightly sensitive to cytotoxicity induced by B[α]P than HepG2 with 10 μM of IC 50 . It was reported that 5 μM of B[α]P reduced the HepG2 cell viability to about 44% [25]. Another study determined the concentration inhibited the cell growth by 20% (IC 20 ) of B[α]P to 8.35 μM by exposing the B[α]P for 48 h to the HepG2 cell [26].…”

“…was measured at 570 nm using a microplate reader (Thermo Scientific, San Jose, CA, USA). The experiment was conducted in triplicate, and the percentage of cell viability was calculated according to a previous study [25].…”

Association of cigarette smoking with neuromyelitis opticaimmunoglobulin G sero-positivity in neuromyelitis optica spectrum disorder

“…28 The mentioned point clarifies why astrocytes play a very significant role in NMOSD, which is referred to as astrocytopathy. 29 It has been indicated that smoking can damage the mentioned cells 30 which probably contribute to the expression of AQP4 and consequently development of antibodies. Moreover, animal studies conducted in this regard verify the mentioned claim.…”

Extracellular vesicles as mediators of the response to respiratory exposures

“…While this makes lungs efficient for enabling gas exchange, it also makes pulmonary tissue highly vulnerable to airborne toxicants. Airborne toxicants may originate from personal exposures such as tobacco smoking (Lee et al 2017), from occupational exposures including nanoparticles, asbestos, and volatile organic chemicals (Kermanizadeh et al 2016, Paciencia et al 2016, Umbright et al 2017, and from environmental exposures such as particulate matter (PM) from outdoor air pollution (Chen and Yang 2018). Chronic exposure to respiratory toxicants substantially increases the risk of developing lung disease, cardiovascular disease (CVD) and cancer (Bartal 2001, Kelly and.…”