Modulation of serum complement levels following exposure to polychlorinated dibenzo-p-dioxins
| Autor: | Kimber L. White, Alice C. Anderson, Helen H. Lysy, J. Ann Mccay |
|---|---|
| Rok vydání: | 1986 |
| Předmět: |
medicine.medical_specialty
Polychlorinated Dibenzodioxins Complement CH50 Administration Oral Toxicology medicine.disease_cause Mice Internal medicine Streptococcus pneumoniae Complement C3b Inactivator Proteins medicine Animals Pathogen Immunosuppression Therapy Pharmacology Innate immune system Chemistry Body Weight Organ Size Complement system Endocrinology Liver Polychlorinated Dibenzo-p-dioxins Acute exposure Complement C3b Female Serum complement Injections Intraperitoneal |
| Zdroj: | Toxicology and Applied Pharmacology. 84:209-219 |
| ISSN: | 0041-008X |
| DOI: | 10.1016/0041-008x(86)90128-6 |
| Popis: | Subchronic 14-day exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) suppressed serum total hemolytic complement activity (CH50) in female B6C3F1 mice at doses of 0.01, 0.05, 0.1, 0.5, 1.0, and 2.0 micrograms/kg. Serum levels of complement component C3 were also suppressed at doses of 0.5, 1.0, and 2.0 micrograms/kg. Another dioxin isomer, 1,2,3,6,7,8-hexachlorodibenzo-p-dioxin (HCDD), also produced dose-dependent suppression of complement activity at doses of 0.1, 1.0, and 10 micrograms/kg with decreased C3 levels at 10 micrograms/kg. Both TCDD and HCDD enhanced susceptibility to Streptococcus pneumoniae, a bacterial pathogen whose host defense is complement mediated. Recovery studies demonstrated that complement activity in TCDD (1 microgram/kg) and HCDD (10 micrograms/kg)-treated animals was suppressed until 50 days post-treatment, while low doses of HCDD (0.1 and 1.0 micrograms/kg) elevated CH50 levels. Acute exposure to TCDD (14 micrograms/kg) also suppressed complement CH50 and C3 levels. These studies demonstrate that the complement system and innate immunity represent potential target sites for polychlorinated dibenzo-p-dioxins. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|