The effects of vitamins C and E on bone marrow chromosomes of the mouse exposed to 1 Gy of whole-body gamma-irradiation were studied. These vitamins, dissolved in water/peanut oil, were administered orally as acute doses, either 2 h before, immediately after, or 2 h after irradiation. Both vitamins significantly reduced the frequencies of micronuclei and chromosomal aberrations in bone marrow cells; radioprotection by vitamin E was, however, appreciably greater than that afforded by vitamin C. Administration of the vitamins to mice immediately after irradiation was as effective as that 2 h before irradiation. A sequential treatment consisting of both these vitamins did not result in additional radioprotection over that afforded by vitamin E alone. The probable mechanisms of radioprotection are discussed.

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The possible role of orally fed Chlorella vulgaris (E-25) in modulating the gamma-ray induced chromosomal damage in whole-body irradiated mice was evaluated using a micronucleus test. Different doses of E-25 were administered either chronically (once, twice or thrice a day for 28 days) or as single acute doses before/after irradiation. A significant radioprotective effect was observed in both acute and chronic pretreatments, but only at doses above 400 mg/kg body weight. However, in mice that received E-25 (500 mg/kg) three times a day for 28 days, there was no protective effect, and a significant loss in their body weight was observed. Interestingly, E-25 afforded significant radioprotection even when it was administered within 0.4 hr after irradiation.

The effect of pretreatment with buthionine sulphoximine (BSO) on the radiosensitivity of mouse bone marrow cells was studied using the in vivo micronucleus test. Varying concentrations of BSO were injected into mice by intraperitoneal injection 2 h before irradiation, and the frequency of micronuclei in polychromatic erythrocytes (MnPCEs) of bone marrow were scored. Treatment with BSO resulted in a significant reduction (41% at 20 mg/kg body weight) in the frequency of micronuclei induced by 1 Gy gamma-rays. Reduction was observed in cells sampled at 24, 30 and 48 h postirradiation with no apparent effect on the ratio of poly- to normo-chromatic erythrocytes in BSO-treated versus control groups. Glutathione levels in the bone marrow of BSO-treated animals 2 h after a single injection were found to be unaltered. The protective effect of BSO was not observed if it was given either immediately or 2 h after irradiation. Based on these and earlier findings it seemed as if BSO molecules may be involved in physicochemical reactions with reactive species generated in the system by irradiation. BSO showed relatively high reaction rate constants with hydroxyl radical (.OH, 2.5 x 10(9) dm3 mol-1s1, calculated on the basis of competition kinetics) and with singlet oxygen (1O2, 4.3 x 10(7) dm3 mol-1s-1 but a lower rate constant with hydrated electrons (< or = 5.0 x 10(6) dm3 mol-1s1). Based on half-life estimates, transients formed and potential for damage to biomolecules, .OH and 1O2 seemed to be the possible species responsible. In vitro studies reveal that BSO has significant abilities to protect DNA against single-strand breaks and lipid peroxidation induced by 1O2 in microsomal membranes. This supports our hypothesis that BSO may be involved in scavenging the reactive species generated and that besides .OH, 1O2 may also be a major player in radiation damage.