Equal amounts of carbon-12 methyl halides and carbon-13 methane, along with hydrogen, have been introduced into a hot-filament diamond CVD chamber. The isotopic ratios of the as-deposited diamond films on tantalum have been measured by Raman spectroscopy. It was found that methyl chloride yielded carbon-12 enriched diamond films, while the other methyl halides resulted in equal amounts of carbon-13 and carbon-12 in the films. Furthermore, the carbon-12 enrichment was more enhanced as the substrate temperature was lowered. Matrix-isolation FTIR analyses of the gas samples collected during the deposition indicated that there was no straightforward agreement between the 12C/13C ratios of the gas phase species, methane and acetylene, and that of the diamond films. The results imply the presence of a new chlorocarbon radical such as CH2Cl, which is postulated as a more effective growth species than the methyl radical.

1. The biochemical basis for the human renal Fanconi syndrome, including glucosuria, phosphaturia and aminoaciduria, remains enigmatic. This is due, in part, to the lack of an appropriate animal model. Since there is an association between the human genetic disease hereditary tyrosinaemia, for which urinary excretion of the compound succinylacetone constitutes a biochemical marker, and a renal Fanconi syndrome, we have examined the relationship between succinylacetone and renal tubular function in the rat. 2. Intraperitoneal injection of succinylacetone for 3 consecutive days into adult male Sprague-Dawley rats resulted in succinylacetone plasma concentration of 3 mmol/l. This concentration was associated with glucosuria, aminoaciduria, polyuria, reduced renal phosphate reabsorption and normal creatinine clearance. In addition, urinary porphobilinogen and total porphyrin excretions were markedly reduced. In animals permitted to recover for 7 days after succinylacetone administration, these renal functional changes remitted partially or completely. Ultrastructural examination of the kidneys after the 3 days of treatment showed no fine structural changes. 3. We conclude that the physiological alterations produced in normal rat renal tubules by succinylacetone provide the basis for the study of the biochemical changes underlying the human renal Fanconi syndrome.

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