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The study investigated the potential oxidative metabolism of nine aromatic amine compounds used in hair dyes using human liver microsomes and hepatocytes. Toluene-2,5-diamine (TDA), p-aminophenol, m-aminophenol, p-methylaminophenol, N,N′-bis(2-hydroxyethyl)-p-phenylenediamine, and 1-hydroxyethyl-4,5-diaminopyrazole showed no evidence of oxidative metabolism. While oxidized metabolites of 4-amino-2-hydroxytoluene (AHT), 2-methyl-5-hydroxyethylaminophenol (MHEAP), and phenyl methyl pyrazolone (PMP) were detected, they did not exhibit NADPH-dependent covalent binding, indicating they were not reactive. Further studies in human hepatocytes revealed that all compounds underwent conjugation without forming oxidative metabolites. The findings suggested that the tested hair dye ingredients did not metabolize into potentially reactive oxidized metabolites in the liver.

The study from 1983 focused on human epidermal transglutaminase, an enzyme crucial for epidermal terminal differentiation. It required calcium or strontium and a free sulfhydryl group, similar to liver transglutaminase, but unlike plasma transglutaminase, it did not need proteolytic activation. The enzyme's activity increased significantly after treatment with organic solvents, heat, and chaotropic reagents, although these treatments did not change its molecular weight or immunologic properties. The research aimed to develop monoclonal antibodies for detailed structural analysis and to explore safe methods for modulating the enzyme's function in human epidermal diseases.

The study created transgenic mice overexpressing the SSAT gene, leading to significant changes in polyamine levels and permanent hair loss, with the liver showing a notable reduction in spermine. Despite high SSAT mRNA levels, enzyme activity increased only moderately unless induced by ZnSO4 or DENSPM, which drastically boosted enzyme activity and depleted liver polyamines, resulting in high mortality and liver damage. This indicated that SSAT overexpression made the mice highly sensitive to polyamine analogues and suggested a post-transcriptional regulation mechanism for SSAT expression involving translational or RNA processing control.

The study involved generating a transgenic mouse line overexpressing the SSAT gene under a mouse metallothionein I promoter, leading to significant changes in tissue polyamine pools and delayed permanent hair loss compared to previous models. The liver was notably affected, with drastic reductions in spermine and increases in putrescine. Despite high levels of SSAT mRNA, enzyme activity was only moderately elevated unless induced by ZnSO4 or the polyamine analogue DENSPM, which caused a massive increase in enzyme activity and depletion of spermidine and spermine pools. This treatment led to high mortality and liver damage, indicating that SSAT overexpression made the mice highly sensitive to polyamine analogues, suggesting a post-transcriptional regulation mechanism.