Studies have shown effects of dietary lipids on carcinogenesis and tumour progression. Different mechanisms for the inhibitory effect of n-3 fatty acids (FA) have been: proposed. The inhibition of the growth of subcutaneously transplanted A427 lung adenocarcinoma cells in athymic nude mice may occur due to an increased level of lipid peroxidation products and is the object of this study. The nude mice were fed diets supplemented with corn oil (CO) olive oil (OO) or K85, a: mixture of ethyl esters of n-3 FAs, mainly eicosapentaenoic acid (EPA, 20:5, n-3) and docosahexaenoic acid (DHA, 22:6, n-3). Tumours of the n-3 FA group showed reduced growth. Peroxidation products measured by the thiobarbituric acid reactive substances (TBARS) test showed higher levels in tumours from n-3 FA fed mice than in the other diet groups. The growth inhibitory effects and the elevated level of TBARS in the n-3 FA diet group were counteracted by vitamin E supplement in the diet. Cu/Zn-superoxide dismutase (SOD) activity in liver did not differ greatly among the diet groups. The Ki-67 labelling index (LI), indicating cell proliferation rate was significantly lower in the K85 diet group compared to the other diet groups.

Experimental evidence suggests that inorganic lead and benzo[a]pyrene (BaP) suppress the development of primordial oocytes during fetal life. We examined the single and combined effects of prenatal exposure to BaP and moderate doses of lead. The fertility and ovarian morphology of F1 female NMRI mice in four treatment groups (nine mice per group) were investigated: control; lead (F0 given 1 g PbCl2/L in drinking water until mating); BaP (10 mg/kg body weight daily by oral intubation on days 7-16 of F0 pregnancy); and combined lead and BaP. F1 groups exposed prenatally to BaP either alone or in combination with inorganic lead showed markedly reduced fertility with few ovarian follicles compared to controls, whereas the group exposed to lead only had measures comparable to the controls. Mice exposed to both lead and BaP had a significantly longer gestation period (days to litter) compared to mice exposed only to BaP, lead, or controls. There is a nonsignificant indication that the compounds together further reduce number of offspring, number of litters, and litter size. These results suggest that lead and BaP have synergistic effects on impairment of fertility. The possibility of synergism may be of human relevance as inorganic lead and BaP are ubiquitous environmental pollutants.

Experimental evidence suggests that inorganic lead may modify mutagenic events. We examined the modifying effect of lead on mutagenic events in late spermatogenesis in the dominant lethal assay. Twelve NMRI male mice were given lead chloride in the drinking water and 12 male mice received tap water without lead chloride. Cyclophosphamide (120 mg/kg b.w., i.p.) was given to six males in the lead treatment group and six males in the tap water group 1 week before mating. This resulted in four treatment groups: control, lead, cyclophosphamide, and lead plus cyclophosphamide. Cyclophosphamide given to the males (with or without lead treatment) reduced the numbers of live implants in mated females. The most prominent effect of cyclophosphamide was an increase of resorbed implants. Females mated to lead exposed male mice showed a nonsignificantly lower frequency of resorptions compared to controls. The results give no support to the hypothesis that inorganic lead may influence the mutagenicity of cyclophosphamide in the dominant lethal test.