Alterations in the humoral immune response and tumor frequencies in mice exposed to benzo[a]pyrene and x‐rays before or after birth
- 19 October 1982
- journal article
- research article
- Published by Taylor & Francis in Journal of Toxicology and Environmental Health
- Vol. 10 (4-5) , 817-835
- https://doi.org/10.1080/15287398209530297
Abstract
Pregnant mice were 1-3 treated mid (11-13 days) or late (16-18 days) gestation with benzo[a]pyrene (BaP) (150 .mu.g/g body weight), 150 R X-irradiation, or X-irradiation + BaP. Virgin mice were injected with BaP after birth (at 1 wk or 16 wk) with doses similar to or higher than those to which progeny of pregnant mice were exposed. The offspring exposed during fetal life showed a marked suppression in anti-SRBC [sheep red blood cell] plaque-forming cells (PFC) 1 wk after birth (pups), followed by an apparent recovery at 4 wk. Return to the immunosuppressed state seen in pups was most noticeable in adults encountering BaP alone during gestation. In this group, increased tumor incidence was associated with a sustained reduction in PFC response. After fetal exposure to X-rays or injection with BaP postnatally, immune competence was not appreciably different from normal in late life and tumor incidence was slightly higher than controls with X-rays or 150 .mu.g/g body weight of BaP. When X-rays were given in conjunction with BaP, it appeared that immune suppression was abated and tumor incidence reduced. The effect of BaP on PFC and tumor incidence varied according to the time in gestation when the carcinogen was given. The liver was the primary target for tumor growths in males. In females, a high incidence of ovarian tumors was seen, but only after mid-gestation exposure. The frequency of lung tumors increased following late gestation insult in both sexes. Susceptibility to injury of different components of the developing humoral immune system and the disposition of the sexes for tumor induction are functions of the gestational time of exposure to BaP. Animals exposed prenatally to the carcinogen are more sensitive to immune suppression and increased tumor incidence than those exposed postnatally. Immune deficiency (suppression) influences the increase in neoplastic expression.Keywords
This publication has 32 references indexed in Scilit:
- Depressed humoral immunity and increased tumor incidence in mice followingin uteroexposure to benzo[a]pyreneJournal of Toxicology and Environmental Health, 1980
- Transplacental action of benzo(a)pyrene and pyreneBulletin of Experimental Biology and Medicine, 1977
- Ly phenotype and mechanism of action of mouse neonatal suppressor T cells.The Journal of Experimental Medicine, 1977
- Differential Effect of Pre- and Postnatal Litter Size Reduction on Body Weight and Development of Stress Response in the RatNeonatology, 1977
- An overview of transplacental chemical carcinogenesisTeratology, 1973
- Immunodepression as a factor during 3‐methylcholanthrene carcinogenesis and subsequent tumour growth in miceInternational Journal of Cancer, 1973
- IN VITRO CYTOTOXICITY BY A NONTHYMUS-PROCESSED LYMPHOCYTE POPULATION WITH SPECIFICITY FOR A VIRALLY DETERMINED TUMOR CELL SURFACE ANTIGENThe Journal of Experimental Medicine, 1972
- Carcinogen-Induced Immune Depression: Absence in Mice Resistant to Chemical OncogenesisScience, 1969
- Immune reactivity prior to development of thymic lymphoma in C57BL miceInternational Journal of Cancer, 1967
- Prolonged Immunosuppression and Tumor Induction by a Chemical Carcinogen Injected at BirthScience, 1966