1,2-Dimethylhydrazine carcinogenesis in CBA male mice prenatally treated with diethylstilbestrol
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Published on: December 19, 2019
V Turusov1, L Trukhanova, D Samoilov
1Institute of Carcinogenesis, N. N. Blokhin Cancer Research Centre, Moscow, Russian Federation.
Abstract:
CBA female mice, at the 17th day of pregnancy, received single intraperitoneal injection of diethylstilbestrol (DES) at the dose of 1 mg/kg body weight (b. w.). Their descentands at the age of 2 months started receiving subcutaneous injections of 1,2-dimethylhydrazine (DMH) at the dose level of 8 mg(base)/kg b. w., total 15 weekly injections. Prenatal DES treatment of male mice considerably accelerated the development and increased the incidence of DMH-induced androgen-dependent renal adenomas and, notably, renal capsule angiosarcomas (RCA). In males receiving prenatal DES (without subsequent DMH-treatment), there was a statistically significant increase of renal adenomas and 9% of RCA were observed which are exceedinly rare in untreated mice. The enhancement of androgen-dependent tumourigenesis may be considered as an indication, even though indirect, of the hyperandrogenization produced in male mice by the prenatal DES treatment.
Insights
Prenatal exposure to diethylstilbestrol (DES) in male mice accelerates cancer development. This study shows DES exposure significantly increases the incidence of renal adenomas and rare renal capsule angiosarcomas (RCA).
Area of Science:
- Endocrinology
- Oncology
- Toxicology
Background:
- Diethylstilbestrol (DES) is a synthetic estrogen with known endocrine-disrupting properties.
- Prenatal exposure to endocrine disruptors can have long-lasting effects on development and disease susceptibility.
- Androgen-dependent tumors are influenced by hormonal status.
Purpose of the Study:
- To investigate the long-term effects of prenatal diethylstilbestrol (DES) exposure on the development of chemically induced tumors in male mice.
- To determine if prenatal DES exposure influences the incidence and development of androgen-dependent renal tumors and other specific cancers.
- To explore the potential link between prenatal DES exposure and altered androgenic status.
Main Methods:
- CBA female mice received a single intraperitoneal injection of diethylstilbestrol (DES) during pregnancy.
- Male offspring were treated with 1,2-dimethylhydrazine (DMH) starting at 2 months of age for 15 weeks.
- Tumor incidence, including renal adenomas and renal capsule angiosarcomas (RCA), was assessed in treated and control groups.
Main Results:
- Prenatal DES treatment significantly accelerated the development and increased the incidence of DMH-induced androgen-dependent renal adenomas in male mice.
- A notable increase in renal capsule angiosarcomas (RCA), a rare tumor type, was observed in male mice exposed to prenatal DES.
- Even without DMH treatment, prenatal DES exposure led to a statistically significant increase in renal adenomas and the occurrence of RCA.
Conclusions:
- Prenatal DES exposure enhances androgen-dependent tumorigenesis in male mice.
- The findings suggest that prenatal DES exposure may induce hyperandrogenization, contributing to increased tumor development.
- This study highlights the potential for endocrine disruptors to increase susceptibility to specific cancers later in life.
