Radiation protectors

BACKGROUND: Iodine intake in Greenland has been hypothesized to exceed 10 times the recommended amount. The transition from a traditional Arctic society may change the iodine intake, but no field studies have been performed. OBJECTIVE: We aimed to ascertain iodine intakes, factors affecting iodine intake in circumpolar populations, and the usefulness of urinary iodine excretion as a biomarker for validation of Inuit food-frequency questionnaires. DESIGN: Data were collected in a cohort study of 4 Greenland population groups: Inuit living in the capital city, the major town, and settlements in East Greenland and non-Inuit. Supplement use and lifestyle factors were evaluated with questionnaires, and dietary habits were ascertained with a food-frequency questionnaire. Iodine was measured in spot urine samples. RESULTS: One percent of the population of Greenland was invited, and the participation rate was 95%. Less than 5% of Inuit but 55% of non-Inuit had urinary iodine excretion < 50 mug/24 h. Median urinary iodine excretion declined with the degree of decrease in the traditional lifestyle: it was 198, 195, 147, and 58 mug/24 h among Inuit in settlements, town, and city and in non-Inuit, respectively (P < 0.001). Participants were divided into diet groups calculated from Inuit food frequency. Iodine excretion decreased with increasing intake of imported foods (P < 0.001). In regression models, type of diet and the subject's lifestyle, sex, weight, ethnicity, and intake of iodine-containing supplements affected urinary iodine excretion. CONCLUSIONS: Circumpolar non-Inuit are at risk of iodine deficiency. Departure from the traditional Inuit diet lowers iodine intake, which should be monitored in Arctic societies. Urinary iodine excretion may be a useful biomarker of traditional Inuit food frequency.

The potential of antioxidants to reduce the cellular damage induced by ionizing radiation has been studied in animal models for more than 50 years. The application of antioxidant radioprotectors to various human exposure situations has not been extensive although it is generally accepted that endogenous antioxidants, such as cellular non-protein thiols and antioxidant enzymes, provide some degree of protection. This review focuses on the radioprotective efficacy of naturally occurring antioxidants, specifically antioxidant nutrients and phytochemicals, and how they might influence various endpoints of radiation damage. Results from animal experiments indicate that antioxidant nutrients, such as vitamin E and selenium compounds, are protective against lethality and other radiation effects but to a lesser degree than most synthetic protectors. Some antioxidant nutrients and phytochemicals have the advantage of low toxicity although they are generally protective when administered at pharmacological doses. Naturally occurring antioxidants also may provide an extended window of protection against low-dose, low-dose-rate irradiation, including therapeutic potential when administered after irradiation. A number of phytochemicals, including caffeine, genistein, and melatonin, have multiple physiological effects, as well as antioxidant activity, which result in radioprotection in vivo. Many antioxidant nutrients and phytochemicals have antimutagenic properties, and their modulation of long-term radiation effects, such as cancer, needs further examination. In addition, further studies are required to determine the potential value of specific antioxidant nutrients and phytochemicals during radiotherapy for cancer.

Acta Oncol. 1994;33(2):139-57.
On radiation damage to normal tissues and its treatment. II. Anti-inflammatory drugs.
Michalowski AS.
MRC Cyclotron Unit, Hammersmith Hospital, London, UK.

In addition to transiently inhibiting cell cycle progression and sterilizing those cells capable of proliferation, irradiation disturbs the homeostasis effected by endogenous mediators of intercellular communication (humoral component of tissue response to radiation). Changes in the mediator levels may modulate radiation effects either by assisting a return to normality (e.g., through a rise in H-type cell lineage-specific growth factors) or by aggravating the damage. The latter mode is illustrated with reports on changes in eicosanoid levels after irradiation and on results of empirical treatment of radiation injuries with anti-inflammatory drugs. Prodromal, acute and chronic effects of radiation are accompanied by excessive production of eicosanoids (prostaglandins, prostacyclin, thromboxanes and leukotrienes). These endogenous mediators of inflammatory reactions may be responsible for the vasodilatation, vasoconstriction, increased microvascular permeability, thrombosis and chemotaxis observed after radiation exposure. Glucocorticoids inhibit eicosanoid synthesis primarily by interfering with phospholipase A2 whilst non-steroidal anti-inflammatory drugs prevent prostaglandin/thromboxane synthesis by inhibiting cyclooxygenase. When administered after irradiation on empirical grounds, drugs belonging to both groups tend to attenuate a range of prodromal, acute and chronic effects of radiation in man and animals. Taken together, these two sets of observations are highly suggestive of a contribution of humoral factors to the adverse responses of normal tissues and organs to radiation. A full account of radiation damage should therefore consist of complementary descriptions of cellular and humoral events. Further studies on anti-inflammatory drug treatment of radiation damage to normal organs are justified and desirable.

BACKGROUND: In I-131-MIBG therapy, I-131-iodide can be released from the I-131-MIBG molecule. Hypothyroidism might result from the undesirable irradiation of the thyroid gland. To prevent this, stable iodide such as potassium iodide (KI) is given to oversaturate the thyroid before I-131-MIBG is administered. PROCEDURE: In the present study, the incidence of hypothyroidism (elevated TSH) was correlated with the thyroidal uptake of I-131 and dose (MIRD dosimetry) after 35 individual treatments in ten patients. Iodine-131-MIBG therapy was performed using a modified dosage of 1.9-11.1 GBq (50-300 mCi) IV. Premedication with KI was done as recommended with a dose of 100 mg KI orally from 2 days before until 4 weeks after I-131-MIBG. RESULTS: The absorbed thyroidal dose amounted to a very variable range of 0.2 (patient # 1) up to 30.0 (patient 3) Gy with 7.1 +/- 7.9 Gy per treatment and 24.1+/- 19.2 Gy per patient (mean+/- SD), despite the same and compliantly taken KI premedication protocol. Up to now, 4/10 or 40% of patients have developed hypothyroidism after a mean follow-up period of 11 months and a mean total administered dose of 18.7 GBq (505 mCi). A trend towards higher thyroidal doses was seen in the hypothyroid patients. CONCLUSIONS: This study observes a general high inter- and intra-individual variability in radio-iodide uptake in the thyroid after I-131-MIBG therapy despite KI premedication, as well as possible occurrence of hypothyroidism. A dose-response relationship needs confirmation on a larger cohort of patients to reach statistical value. An alternative thyroid cytoprotection strategy for possible long-term survivors may be considered.