Alkylnaphthalene. XI. : Pulmonary Toxicity of Naphthalene, 2-Methylnaphthalene, and Isopropylnaphthalenes in Mice

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Pulmonary toxicity of naphthalene (NAP), 2-methylnaphthalene(2-MN), 2-isopropylnaphthalene (2-IPN) and 2,6-diisopropylnaphthalene (2,6-DIPN) was studied in mice. Twenty four h after the intraperitoneal (i.p.) administration of NAP (200mg/kg (1.6mmol)) or 2-MN (400mg/kg (2.8mmol)), pulmonary damage was detected. Prior treatment with diethyl maleate resulted in enhancement of NAP and 2-MN-induced bronchiolar damage. In contrast to the effects of NAP and 2-MN, injections of 2-IPN (3000mg (17.6mmol)/kg) and 2,6-DIPN (3000mg (14.2mmol)/kg) did not cause detectable pulmonary damage. Injections of NAP and 2-MN caused considerable depletion of pulmonary reduced glutathione (GSH), while injections of 2-IPN and 2,6-DIPN caused only a slight depletion. There were general decreases in the binding of the compounds to lung slices with increasing number of carbons of the alkyl substituent. Pretreatment with a cytohrome P-450 inducer (β-naphthoflavone) increased the binding of NAP, 2-MN, and 2-IPN to lung slices.Treatments with NAP, 2-MN, 2-IPN and 2,6-DIPN did not affect the lipid peroxidation or phospholipid contents in the lung.These results suggest that the difference in pulmonary toxicity among NAP, 2-MN, 2-IPN, and 2,6-DIPN may be dependent on the ability of these compounds to irreversibly bind to lung tissue.
社団法人日本薬学会の論文
1990-11-25