ABSTRACT
Insertion of the transposon Tn5 into the T-region of the octopine Ti plasmid of Agrobacterium tumefaciens gives rise to crown gall tumors having altered morphology. Three loci within the T-DNA that control tumor morphology have been detected [Garfinkel, D. J., Simpson, R. B., Ream, L. W., White, F. F., Gordon, M. P. & Nester, E. W. (1981) Cell 27, 143-153]. They influence tumor size (tml), production of roots (tmr), or production of shoots (tms). Cytokinin and auxin levels in such mutant tumors were examined by HPLC/radioimmunoassay and HPLC/fluorescence assay, respectively. Free indoleacetic acid levels (in pmol/g) were: uninfected tobacco stem tissues, 128; wild-type A348 tumors, 295; tml mutant tumors, 307; tmr mutant tumors, 129; and tms mutant tumors, 70. Average trans-ribosylzeatin levels were correspondingly: 0.97, 48, 40, 0.54, and 1,400 pmol/g. trans-Ribosylzeatin/indoleacetic acid ratios were as high as 24 in shoot-producing tumors and as low as 0.003 in root-producing tumors. The evidence strongly suggests that tumor phytohormone levels are determined by genes in the T-DNA.
ABSTRACT
Enzymatically isolated hepatocytes were utilized to evaluate levels of lipid peroxidation in young (3 months), adult (12 months) and aged (25 months) Fisher-344 female rats. Lipid peroxidation was measured by assaying levels of malonaldehyde, a by-product of the peroxidation reaction. Young, adult and aged animals were fed a liquid antioxidant-free diet for 21 days prior to the hepatocyte isolation. Cells isolated from young rats demonstrated the highest levels of lipid peroxidation (microgram of malonaldehyde/10(6) cells). This increase may be a result of the isolation procedure or of metabolic differences found in younger animals. When hepatocytes from aged animals on the antioxidant-free diet were incubated in the presence of lipid peroxidation inducers, such as cumene hydroperoxide or NADPH, significant elevations in lipid peroxidation over comparable adult values were observed. Aged hepatocytes appear to be more susceptible to the peroxidation process than adult hepatocytes, possibly due to defective peroxidation defenses.
