PubMed · 5048057
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1972. Chromosome methodologies in mutation testing.. https://doi.org/10.1016/0041-008x(72)90177-9
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The influence of methylmercury on the developing immune system was studied in offspring from Balb/c mice exposed to 0, 0.5 or 5 mg Hg/kg as methylmercury in the diet. Dams were exposed for 10 weeks prior to mating, during gestation and lactation. Pups were exposed to mercury until day 15 of lactation, thereafter the pups were given control milk and control diet. Samples for mercury analysis were collected from the pups on days 22 and 50, and for immunological studies on days 10, 22 and 50. The exposure resulted in significantly increased total Hg concentrations in whole blood on day 22 and 50 in offspring from the 5 mg Hg/kg group, and in offspring from the 0.5 mg Hg/kg group on day 22. On day 50, blood mercury levels had decreased to background levels in the 0.5 mg Hg/kg group. Increased numbers of splenocytes and thymocytes were found in offspring from the 0.5 mg Hg/kg group. Flow cytometry analysis of thymocytes revealed increased numbers and altered proportions of lymphocyte subpopulations within the thymus in offspring from both of the exposed groups. The proliferative response of splenocytes to the B-cell mitogen LPS was increased in offspring from dams exposed to 5 mg Hg/kg, and the primary antibody response to a viral antigen was stimulated in pups from dams exposed to 0.5 mg Hg/kg. The present results indicate that placental and lactational transfer of mercury affects thymocyte development and stimulates certain mitogen- or antigen-induced lymphocyte activities in mice.
We examined the effects on dominant lethality, the incidence of fetal abnormalities and tumour incidence in surviving offspring of acute and subchronic exposure of male mice by inhalation to the industrial monomer, 1,3-butadiene. In the acute study, CD-1 mice were exposed to atmospheres containing 0 (n = 25), 1250 (n = 25) or 6250 ppm (n = 50) for 6 h, and each male was caged 5 days later for 1 week with two untreated virgin females. One of the females was killed humanely on day 17 of gestation. The other was allowed to deliver and rear her litter and the litters were monitored throughout adulthood. The killed female was examined for the number of live foetuses, the number of post implantation deaths (early and late) and the number and type of any gross malformations. In the subchronic study, males were exposed to 0 (n = 25), 12.5 (n = 25) or 1250 (n = 50) for 6 h per day on 5 days per week for 10 weeks and then mated the next morning. Mating and observation details were as for the acute study. Acute exposure to butadiene resulted in only a small decrease in implantations; after 10 weeks' subchronic exposure with either the high or low concentration, however, a wide variety of statistically significant effects was seen. At 1250' ppm, the number of implantations was reduced, dominant lethal mutations were induced, and the incidences of early and late deaths were increased; some of the live foetuses were malformed. The low dose also increased the frequency of malformations and late deaths but it did not affect the number of early deaths. Skeletal examination of malformed foetuses, randomly selected normal litter mates and controls confirmed the abnormalities seen at necropsy in malformed foetuses. However, karyotypic analysis of foetal liver from malformed foetuses, randomly selected normal litter mates and controls showed no karyotypic abnormalities. The number of gross suspected tumours in the F1 adults did not appear to reveal an increase over control values. Thus, butadiene is mutagenic in the germ cells of male mice, as shown by the induction of dominant lethality at 1250 ppm, and the frequencies of late deaths and congenital malformations appear to be increased at the subchronic level of 12.5 ppm and skeletal examination of malformed foetuses confirmed the macroscopic abnormalities.
Great Lakes waterbird populations have experienced less-than-expected hatchability of eggs and a greater-than-expected incidence of developmental abnormalities. Such deleterious effects have been attributed to polyhalogenated hydrocarbons such as polychlorinated biphenyls (PCBs). PCBs are of primary concern since they are present in significant quantities in the environment. Specific PCB congeners, 3,3',4,4',5-pentachlorobiphenyl (IUPAC number 126), 3,3',4,4'-tetrachlorobiphenyl (IUPAC number 77), and 2,3,3',4,4'-pentachlorobiphenyl (IUPAC number 105), were injected (singly or in combination) into the yolks of White Leghorn chicken (Gallus domesticus) eggs prior to incubation. Teratogenicity was assessed in dead embryos and in hatchlings. Hatchlings were raised for 3 wk to assess body weight gain and mortality. At the end of the 3-wk period, chicks were subjected to necropsy and the brain, bursa, heart, liver, spleen, and testes were removed and weighed. All 3 congeners caused increased embryo mortality, with approximately 50% mortality occurring at 0.6, 8.8, and 5592 micrograms/kg egg for congeners 126, 77, and 105, respectively. All three congeners also produced significantly more abnormalities than the vehicle. Chicks from PCB-injected eggs had lower body weights at wk 2 and 3 of age. Congener 126 caused lower relative bursa weights, congener 77 caused greater relative spleen weights and lower relative liver weights, and all three congeners caused relative heart weights to be greater when compared to control.