Abstract
Naphthalene causes mouse airway epithelial injury. However, repeated exposures of naphthalene result in mouse airway tolerance. Previous results showed that toxicity or tolerance was correlated with changes of phosphorylcholine-containing lipids. In this study, a mass spectrometry-based lipidomic approach was applied to examine the effects of naphthalene-induced injury or tolerance in the male ICR mice. The injury model was vehicle x 7 plus 300 mg/kg naphthalene while the tolerant one was 200 mg/kg daily x 7 followed by 300 mg/kg naphthalene on day 8. The lung, liver, kidney, and serum samples were collected for profiles of phosphorylcholine-containing lipids including phosphatidylcholines (PCs) and sphingomyelins (SMs). A partial least-square-discriminate analysis model showed different lung phosphorylcholine-containing lipid profiles from the injured, tolerant, and control groups. Perturbation of diacyl-PCs and plasmenylcholines may be associated with enhanced membrane flexibility and anti-oxidative mechanisms in the lungs of tolerant mice. Additionally, alterations of lyso-PCs and SMs may be responsible for pulmonary dysfunction and inflammation in the lungs of injured mice. Moreover, serum PC(16:0/18:1) has potential to reflect naphthalene-induced airway injuries. Few phosphorylcholine-containing lipid alterations were found in the mouse livers and kidneys across different treatments. This study revealed the changes in lipid profiles associated with the perturbations caused by naphthalene tolerance and toxicity; examination of lipids in serum may assist biomarker development with the potential for application in the human population.
Highlights
Naphthalene, the most common polycyclic aromatic hydrocarbon (PAH), is present in both air and groundwater from a variety of sources, such as industrial plants, vehicle traffic, and forest fires [1, 2]
The variations of phosphorylcholine-containing lipid profile among three treatments from the analysis of mass spectrometry (MS) spectra on mouse lungs were further analysed in a partial leastsquare-discriminate analysis (PLS-DA) model (R2Y = 0.95; Q2 = 0.81)
Naphthalene-induced respiratory toxicity or tolerance was correlated with changes in phosphorylcholine-containing lipids were suggested by our previous 1H NMR-based metabolomic approach
Summary
Naphthalene, the most common polycyclic aromatic hydrocarbon (PAH), is present in both air and groundwater from a variety of sources, such as industrial plants, vehicle traffic, and forest fires [1, 2]. Moth repellents, cigarette smoking, deodorant and furniture release certain amounts of naphthalene [3]. Studies have shown that naphthalene can be detected in various tissues and organs from farm animals and human bodies [4,5,6,7]. Previous studies showed naphthalene induced respiratory toxicity in a mouse model. After mice received a single dose of naphthalene (200 mg/kg, i.p.), non-ciliated, bronchiolar epithelial (Clara) cells in the airway were injured, whereas there was no obvious tissue damage in the liver or kidney [8]. Another study further illustrated naphthalene-induced intracellular changes, including membrane bleb formation, a swollen smooth endoplasmic reticulum, swollen mitochondria with granular matrices, cytoskeletal filament rearrangements, and increased membrane permeability on injured terminal bronchiolar Clara cells [9]
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