Metabolism and nephrotoxicity of indan in male Fischer 344 rats.

Indan, a component of fuels, solvents, and varnishes, is metabolized in male Fischer 344 rats to 1-indanol, 2-indanol, 5-indanol, 1-indanone, 2-indanone, 2-hydroxy-1-indanone, cis-1,2-indandiol, and trans-1,2-indandiol. The metabolites were identified using the techniques of gas chromatography (GC) and gas chromatography/mass spectrometry (GC/MS). The rats treated with indan demonstrated the classic lesions of hydrocarbon-induced nephropathy. The kidney damage produced was less than that found for tetralin and other branched-chain acyclic hydrocarbons.

The metabolism of t-butylcyclohexane in Fischer-344 male rats with hyaline droplet nephropathy.

The molecule t-butylcyclohexane is one of the first examples of a branched alkyl group attached to a hydrocarbon ring shown to be capable of producing renal damage at the corticomedullary junction of male rats. A metabolic study of t-butylcyclohexane yielded the following urinary metabolites: trans-4-t-butylcyclohexanol, 2c-hydroxy-4t-t-butylcyclohexanol, 2-methyl-2-cyclohexylpropanoic acid, 2c-hydroxy-4c-t-butylcyclohexanol, 2-methyl-2-cyclohexyl-1,3-propanediol, 2t-hydroxy-4t-t-butylcyclohexanol, and cis -4-t-butylcyclohexanol. As with other hydrocarbons of similar molecular weight that induce nephropathy in male rats, preferential sites of oxidative metabolism were observed that could potentially be related to the pathogenesis.

Gas chromatographic/mass spectrometric studies of the urinary metabolites of male rats given indan.

The identified urinary metabolites of male rats exposed to indan are: 1- and 2-indanone; 1-, 2- and 5-indanol; 2- and 3-hydroxyl-1-indanone; and cis- and trans-indan-1,2-diol. Indan causes kidney damage in male rats in a manner similar to the cyclic hydrocarbons cis- and trans-decalin and JP-10. Lesions produced by indan occur only in male rats and not in female or control rats.