Physical inactivity of murine retrovirus infected C57BL/6 mice is prevented by melatonin and dehydroepiandrosterone

Mohsen Araghi-Niknam, Lisa Lane, Ronald R Watson

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

LP-BM5 retrovirus infection and hormone synthesis modulate many physiological systems that could affect physical activity. Infection induced oxidative damage and immunodeficiency of female mice which hormone supplement prevented. Therefore, the effects of retrovirus infection and hormone supplementation were assessed on physical activity using a computerized video system. Retroviral infection increased activity when stationary while lowering average speed and resting time. Hormone supplementation partially modified changes due to murine AIDS. Dehydroeplandrosterone (DHEA) or melatonin (MLT) supplementation restored the average speed; ambulatory time and distance traveled of retrovirus infected mice. MLT as well as the combination of DHEA + MLT increased body movement, but decreased average speed and distance traveled. Thus, retrovirus infection had significant effects on physical activity. Further studies into the relationship between the DHEA and/or MLT and physical activity will assert the contribution of these hormones to the treatment of murine AIDS.

Original languageEnglish (US)
Pages (from-to)144-148
Number of pages5
JournalProceedings of the Society for Experimental Biology and Medicine
Volume219
Issue number2
StatePublished - Nov 1998

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Dehydroepiandrosterone
Melatonin
Retroviridae
Inbred C57BL Mouse
Retroviridae Infections
Hormones
Murine Acquired Immunodeficiency Syndrome
Infection

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Physical inactivity of murine retrovirus infected C57BL/6 mice is prevented by melatonin and dehydroepiandrosterone. / Araghi-Niknam, Mohsen; Lane, Lisa; Watson, Ronald R.

In: Proceedings of the Society for Experimental Biology and Medicine, Vol. 219, No. 2, 11.1998, p. 144-148.

Research output: Contribution to journalArticle

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