Nitronaphthalene appears as a yellow crystalline solid. Insoluble in water and denser than water. May irritate skin and eyes. Readily ignitable and may be difficult to extinguish once ignited. Used to make dyes and other chemicals.
颜色/状态：
Pale yellow needles
气味：
Odorless
闪点：
327 °F (NTP, 1992)
溶解度：
In water, 9.18 mg/l @ 25 °C
蒸汽密度：
5.96 (NTP, 1992) (Relative to Air)
蒸汽压力：
4.8X10-4 mm Hg @ 25 °C
亨利常数：
1.76e-06 atm-m3/mole
大气OH速率常数：
5.40e-12 cm3/molecule*sec
分解：
When heated to decomposition it emits toxic fumes of /nitrogen oxides/.
Incubation of 1-nitronaphthalene under anaerobic conditions with a postmitochondrial supernatant from the livers of male Fischer rats resulted in the stoichiometric formation of 1-naphthylamine. Under aerobic conditions, a rat liver metabolic system converted 1-nitronaphthalene into dihydrodiol and phenol metabolites.
N-Hydroxy-1-naphthylamine (which has been shown to induce tumors in experimental animals) has been detected as a metabolite of 1-nitronaphthalene in vitro.
1-Nitronaphthalene and its reactive products specifically targets the airway epithelium. Its toxicity is synergized by prior long-term ozone exposure. 1-NN appears to specifically target peroxiredoxin 6 and biliverdin reductase as well as the N-terminal region of calreticulin.
Evaluation: There is inadequate evidence for the carcinogenicity in experimental animals of 1-nitronaphthalene. No data were available from studies in humans on the carcinogenicity of 1-nitronaphthalene. Overall evaluation: 1-Nitronaphthalene is not classifiable as to its carcinogenicity to humans (Group 3).
After i.p. administration of (14)C1-NN (100 mg/kg; 60 microCi/kg) /to male Sprague Dawley rats/, 84% of the dose was eliminated in the urine and feces by 48 hr. At 96 hr, 60% of the dose was recovered in the urine, 32% in the feces, and 1% collectively in the tissues, blood, and gastrointestinal contents. The terminal phase rate constant (k(term)) of 1-NN was 0.21 hr(-1), the terminal phase half-life (T(1/2,term)) was 3.40 hr, and the systemic bioavailability was 0.67. When administered i.v. (10 mg/kg; 120 microCi/kg), 85% of the dose was eliminated in the urine and feces by 24 hr. At the end of the study (96 hr), 56% of the dose was recovered in the urine, 36% in the feces, and 1% collectively in the tissues, blood, and gastrointestinal contents. Interestingly, 88% of the dose was secreted into bile by 8 hr. The k(term) was 0.94 hr(-1) and the T(1/2,term) was 0.77 hr.
Lung and liver microsomes from male Swiss-Webster mice metabolized 1-nitronaphthalene to products that bound microsomal macromolecules. The binding was NADPH- and oxygen-dependent and was inhibited by carbon monoxide, nitrogen and SKF-525A. Little binding was detected with kidney microsomes. Pretreatment of the mice with beta-naphthoflavone enhanced the binding to lung microsomal macromolecules; phenobarbital pretreatment increased the binding to liver microsomes. Incubations were also conducted with lung slices and isolated lung cells. Autoradiographs of the lung slices showed that most of the binding occurred in the epithelial cells of the bronchioles and smaller airways. With the isolated lung cells, there was preferential binding of 1-nitronaphthalene to cell populations enriched in Clara cells. beta-Naphthoflavone pretreatment increased the binding of 1-nitronaphthalene in both the lung slices and isolated lung cells.
