ArticleToxicologic pathology2017
A Black Cohosh Extract Causes Hematologic and Biochemical Changes Consistent with a Functional Cobalamin Deficiency in Female B6C3F1/N Mice.
Article in Toxicologic pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Review of black cohosh-induced toxicity and adverse clinical effects.Journal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025Review
- Combined Exposures and Mixtures Research: An Enduring NIEHS Priority.Environmental health perspectives · 2024Article
- A cross-sectional clinical study in women to investigate possible genotoxicity and hematological abnormalities related to the use of black cohosh botanical dietary supplements.Environmental and molecular mutagenesis · 2022Article
- Actein contributes to black cohosh extract-induced genotoxicity in human TK6 cells.Journal of applied toxicology : JAT · 2022Article
- Mechanistic Evaluation of Black Cohosh Extract-Induced Genotoxicity in Human Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Evidence for an Aneugenic Mechanism of Action for Micronucleus Induction by Black Cohosh Extract.Environmental and molecular mutagenesis · 2019Article
- Evaluating Sufficient Similarity of Botanical Dietary Supplements: Combining Chemical and In Vitro Biological Data.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Black cohosh extracts and powders induce micronuclei, a biomarker of genetic damage, in human cells.Environmental and molecular mutagenesis · 2018Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Black cohosh rhizome, available as a dietary supplement, is most commonly marketed as a remedy for dysmenorrhea and menopausal symptoms. A previous subchronic toxicity study of black cohosh dried ethanolic extract (BCE) in female mice revealed a dose-dependent ineffective erythropoiesis with a macrocytosis consistent with the condition known as megaloblastic anemia. The purpose of this study was to investigate potential mechanisms by which BCE induces these particular hematological changes. B6C3F1/N female mice (32/group) were exposed by gavage to vehicle or 1,000 mg/kg BCE for 92 days. Blood samples were analyzed for hematology, renal and hepatic clinical chemistry, serum folate and cobalamin, red blood cell (RBC) folate, and plasma homocysteine and methylmalonic acid (MMA). Folate levels were measured in liver and kidney. Hematological changes included decreased RBC count; increased mean corpuscular volume; and decreased reticulocyte, white blood cell, neutrophil, and lymphocyte counts. Blood smear evaluation revealed increased Howell-Jolly bodies and occasional basophilic stippling in treated animals. Plasma homocysteine and MMA concentrations were increased in treated animals. Under the conditions of our study, BCE administration caused hematological and clinical chemistry changes consistent with a functional cobalamin, and possibly folate, deficiency. Further studies are needed to elucidate the mechanism by which BCE causes increases in homocysteine and MMA.
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