Beta-glucan inhibits the genotoxicity of cyclophosphamide, adriamycin and cisplatin

Amany A Tohamy1, Akmal A El-Ghor, Soheir M El-Nahas

  • 1Zoology Department, Faculty of Science, Helwan University, Cairo, Egypt.

Mutation Research
|October 22, 2003
PubMed

Insights

Beta-glucan (betaG) protects against chromosomal damage caused by chemotherapy drugs like cisplatin. This biological response modifier reduces genotoxicity and restores cell activity, aiding cancer treatment.

Area of Science:

  • Pharmacology and Toxicology
  • Cancer Biology
  • Immunology

Background:

  • Chemotherapy drugs can induce genotoxicity, causing chromosomal aberrations in bone marrow and spermatogonial cells.
  • Biological response modifiers like beta-glucan (betaG) are known for their immunopotentiating effects.
  • Investigating the protective role of betaG against chemotherapy-induced genotoxicity is crucial for improving cancer treatment outcomes.

Purpose of the Study:

  • To investigate the inhibitory effects of beta-glucan on chromosomal aberrations induced by anti-neoplastic drugs.
  • To evaluate the protective potential of beta-glucan in bone marrow and spermatogonial cells.
  • To explore the mechanisms underlying beta-glucan's protective effects against chemotherapy-induced genotoxicity.

Main Methods:

  • Mice were pre-treated with beta-glucan (100 mg/kg bw, i.p.) before administration of anti-neoplastic drugs: cyclophosphamide (CP), adriamycin (ADR), or cisplatin.
  • Chromosomal aberrations were scored in bone marrow and spermatogonial cells.
  • Mitotic activity of bone marrow cells was assessed.

Main Results:

  • Beta-glucan pre-treatment significantly reduced chromosomal aberrations induced by CP, ADR, and cisplatin in both bone marrow and spermatogonial cells.
  • The percentage reduction in aberrations ranged from 26.9% to 57.7% in bone marrow and 44.4% to 57.1% in spermatogonial cells.
  • Beta-glucan also restored the suppressed mitotic activity of bone marrow cells.

Conclusions:

  • Beta-glucan exhibits significant protective effects against chemotherapy-induced genotoxicity.
  • Beta-glucan's free-radical scavenging ability likely contributes to its protective mechanism.
  • These findings suggest beta-glucan can mitigate genotoxicity associated with anti-neoplastic drugs, complementing its immunomodulatory role in cancer therapy.

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Drugs that Destabilize Microtubules01:10

Drugs that Destabilize Microtubules

Microtubules are dynamic structures and can be regulated by microtubule targeting agents (MTAs). Microtubule destabilizing drugs are a class of MTAs that destabilize and prevent microtubules' polymerization. Both natural and synthetic chemicals can be found under this class of drugs. Vincristine and vinblastine, two vinca alkaloids, and colchicine were among the first to be discovered. These drugs can affect cells in various ways, either by inducing a change in cell morphology, preventing...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
Inhibitors of Bacterial DNA Synthesis01:28

Inhibitors of Bacterial DNA Synthesis

Bacterial pathogens depend on precise and efficient DNA replication to sustain infection. Two type II topoisomerases—DNA gyrase and topoisomerase IV—are critical to this process, as they resolve DNA supercoiling and unlink chromosomes during replication. Fluoroquinolones, synthetic derivatives of quinolones, exploit this mechanism by stabilizing the transient DNA–enzyme cleavage complex, preventing strand religation, and causing lethal double-strand breaks. These antibiotics are selectively...
Drugs that Stabilize Microtubules01:15

Drugs that Stabilize Microtubules

Microtubules are dynamic structures that undergo cycles of catastrophe and rescue. The microtubules play a central role in cell division by forming the spindle apparatus for segregating the chromosomes. This makes them ideal targets for regulating dividing cells in tumors and malignant cancer cells. Microtubule stabilizing drugs help stabilize the microtubule formation and promote its polymerization. Paclitaxel was the first microtubule stabilizing agent used as anticancer drug in chemotherapy...