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Effect of selenium on virally induced and transplantable tumor models

Federation Proceedings
|June 1, 1985
PubMed

Insights

Selenium (Se) effectively inhibits tumors, with higher intake needed for maximal effect. Its efficacy varies by tumor type, form, and administration, potentially linked to selenodiglutathione.

Area of Science:

  • Oncology
  • Biochemistry
  • Nutritional Science

Background:

  • Selenium (Se) is a trace element with known biological functions.
  • Glutathione peroxidase (EC 1.11.1.9) is a key antioxidant enzyme.
  • Tumorigenesis involves complex cellular processes influenced by nutritional factors.

Purpose of the Study:

  • To investigate the antitumorigenic effects of selenium.
  • To determine the optimal intake levels of selenium for tumor inhibition.
  • To explore the mechanisms underlying selenium's anti-cancer properties.

Main Methods:

  • Administration of varying quantities and forms of selenium.
  • Assessment of tumor growth inhibition in different tumor models (virally induced and transplantable).
  • Evaluation of glutathione peroxidase activity and selenium metabolism intermediates.

Main Results:

  • Selenium demonstrated effectiveness in inhibiting both virally induced and transplantable tumors.
  • Maximal tumor inhibition required selenium intake exceeding levels for optimal growth and glutathione peroxidase activity.
  • Tumor cell line sensitivity to selenium varied, and efficacy depended on the form and mode of administration.
  • Total tumor mass influenced selenium's effectiveness.

Conclusions:

  • Selenium exhibits significant antitumorigenic potential.
  • Optimal therapeutic outcomes with selenium necessitate higher intake levels and specific administration strategies.
  • Selenodiglutathione or related metabolites are implicated as the active agents responsible for selenium's anti-cancer effects.

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