An evaluation of acetone extracts from six plants in the AMES mutagenicity test

White, Randy; Krumperman, Paul H.; Cheeke, P. R.; Buhler, Donald R.

doi:10.1016/0378-4274(83)90164-9

Cited by 16 publications

(11 citation statements)

References 13 publications

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“…ATS are reported to be free of the SLE-inducing substance that is present in the seeds (Malinow et al, 1982c). Negative results were documented for M. sativa when tested for mutagenicity using Salmonella strains TA98 and TA100 (White et al, 1983).…”

Section: Toxicity/side-effectsmentioning

confidence: 99%

Phytochemical and pharmacological potential ofMedicago sativa: A review

Bora¹,

Sharma²

2010

Pharmaceutical Biology

138

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Section: Toxicity/side-effectsmentioning

confidence: 99%

Phytochemical and pharmacological potential ofMedicago sativa: A review

Bora¹,

Sharma²

2010

Pharmaceutical Biology

138

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“…It is possible that the mutagenic activity of SA relates to this same property of SA to interact and form adducts with DNA. For instance, because SA is an acetone derivative, it may possess some of the properties of acetone, which has been reported to induce mutagenicity in Salmonella typhimurium strains TA 98 and TA 100 in the presence of rat liver microsomes by the Salmonella/mammalian microsome mutagenicity test (Ames Test) (White et al, 1983).…”

Section: Discussionmentioning

confidence: 99%

Increased mutant frequencies in the HPRT gene locus of leukemia HL-60 cells treated with succinylacetone

et al. 2006

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Succinyl acetone (SA) was initially identified in the urine of patients with tyrosinemia type I, an autosomally recessive inherited disease. SA has been used to downregulate the activity of myeloperoxidase (MPO) through its specific inhibition of heme biosynthesis and to investigate the biological properties of MPO in the human myeloid leukemic (HL-60) cell line. The goal of this study is to evaluate the mutagenic potential of SA by determining the frequencies of somatic mutations in the hypoxanthine-guanine phosphoribosyl transferase (HPRT) reporter gene in HL-60 cells following treatment with the chemical. Treatments of HL-60 cells with 500 micromol/L SA for 72 h, a condition generally used to inhibit the MPO activity, resulted in a significantly increased HPRT mutant frequency (HPRT-Mf), compared with the control of untreated cells (47.25 x 10(-6) versus 7.5 x 10(-6), respectively, p <0.01). Treatment of the cells with lower doses of SA also led to an increase in HPRT-Mf but this was significant only with 200 micromol/L (28.67 x 10(-6), p<0.05) and not with doses lower than 100 micromol/L (p0.05), compared with the control of untreated cells (7.5 x 10(-6)). These data show a dose-response increase in HPRT-Mf in HL-60 cells treated with SA, suggesting that this chemical causes mutations in the HPRT locus in these cells either directly or indirectly through its inhibition of the MPO activity.

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“…In addition, one pure acetone extract (Ac-p) was prepared from a mixture of SJ-1 and SI-1 (85/15 w/w) as described by White et al [34] by shaking 60 g of dry plant material with 300 mL acetone for 48 h. The extract was subsequently processed as described above.…”

Section: Preparation Of Plant Extractsmentioning

confidence: 99%

“…In an early study by White et al [34], it was demonstrated that acetone extracts of Senecio jacobaea (common or tansy ragwort) tested positive in the Salmonella/microsome mutagenicity test in the presence of liver S9 preparations, while extracts without the S9 mix caused general toxicity. In a follow-up study, White et al [35] showed again that an acetone extract of common ragwort was positive in the Salmonella mutagenicity test with S9.…”

Section: Introductionmentioning

confidence: 98%