Open AccessShort-term E-cigarette toxicity effects on brain cognitive memory functions and inflammatory responses in mice
Author(s) -
Eka Sunarwidhi Prasedya,
Yogi Ambana,
N. W. R. Martyasari,
Ye’muh Aprizal,
Nurrijawati,
Sunarpi
Publication year - 2020
Publication title -
toxicological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.872
H-Index - 30
eISSN - 2234-2753
pISSN - 1976-8257
DOI - 10.1007/s43188-019-00031-3
Subject(s) - neurotoxicity , proinflammatory cytokine , medicine , neuroinflammation , toxicity , oxidative stress , nicotine , hippocampus , brain damage , hippocampal formation , pharmacology , physiology , pathology , inflammation , endocrinology
Exposure to cigarette smoke (CS) is associated with an increased risk of several neurological diseases such as stroke, Alzheimer's disease, and dementia. At present, commercialization of E-cigarettes (ECs) is increasing, and they are advertised as a less harmful nicotine-delivery system. There are, however, limited studies regarding the neurotoxicity effects of ECs on the brain, which remains a subject of debate. In the present study, we aimed to evaluate the in vivo effects of short-term EC vapor exposure on the brain and compare them with the effects of cigarette smoke (CS). BALB/c mice were exposed to air, CS, and EC for 14 days. We then assessed the inflammatory responses, oxidative stress, and cognitive functions of the mice by using maze tests. Cognitive spatial tests showed that the mice exposed to CS and ECs had delayed time in finding food rewards. EC exposure demonstrated no improvement in spatial memory learning to find the food reward on the next day. This implies that CS and EC exposure possibly causes damage to the olfactory system. Notably, EC exposure potentially causes abnormalities in mice memory functions. Histological staining of the cerebral cortex of mice brain in the EC-exposed group demonstrated inflammatory responses such as necrosis and cytoplasm vacuolization. Immunohistochemical staining revealed high expression of proinflammatory cytokine TNF-α in both the EC- and CS-exposed groups. Hence, we conclude that ECs share similar toxicity profiles as CS, which potentially negatively impact brain function.