Pulmonary Toxicity of 2-Isopropylnaphthalene and Its Photoproducts

• Published in: Eisei kagaku Vol. 37; no. 4; pp. 300 - 306
• Main Authors: KIYOZUMI, MORIO, KOJIMA, SHOJI, HONDA, TOSHIYA, MOTOYAMA, MIWAKO
• Format: Journal Article
• Language: English; Japanese
• Published: The Pharmaceutical Society of Japan 1991
• Subjects: 2-isopropylnaphthalene; binding of lung slice; Clara cell; phospholipid; photoproducts; pulmonary toxicity; reduced glutathione; tissue distribution
• ISSN: 0013-273X
• DOI: 10.1248/jhs1956.37.300

Pulmonary toxicity of 2-isopropylnaphthalene (2-IPN) and its photoproducts was studied in mice. Twenty-four h after the intraperitoneal injection of 2-IPN or its photoproducts, 2-isopropenylnaphthalene (2-IPeN) (1000 mg/kg), 2-acetonaphthone (2-AN) (700 mg/kg), β-naphthol (BN) (50 mg/kg), phthalide (PH) (500 mg/kg) and phthalic acid (PA) (100 mg/kg) produced pulmonary damage, but 2-IPN (3000 mg/kg) and 2-(2-naphthyl)-2-propanol (2-NP) (1000 mg/kg) did not produce pulmonary damage. The maximum levels of 2-IPN in the lung, liver and kidney were observed 6 h after the administration, and then the levels decreased with time. The concentrations of 2-IPeN, 2-NP, 2-AN, BN, PH and PA in the tissues reached the maximum levels within 1 or 2 h, and then rapidly decreased with time. The binding of both 2-AN and BN to lung slices was greater than that of other compounds. The injections of 2-IPN, 2-IPeN, BN and PH caused considerable depletion of pulmonary GSH (reduced glutathione) at 12 h after the administration of the compounds. These results suggested that their reactive metabolites such as "epoxides" were produced and interacted with GSH. While the injection of 2-NP, 2-AN and PA did not cause depletion of pulmonary GSH. Treatment with 2-IPN and its photoproducts did not affect lipid peroxidation and phospholipid in the lung.