Diet and Apoptosis

W. H. Watson, Jiyang Cai, D. P. Jones

Research output: Contribution to journalArticle

86 Citations (Scopus)

Abstract

A range of compounds in or derived from the diet modulates apoptosis in cell cultures in vitro. These observations have important implications concerning the mechanisms whereby dietary components affect health. Proapoptotic compounds could protect against cancer by enhancing elimination of initiated, precancerous cells, and antiapoptotic compounds could promote tumor formation by inhibiting apoptosis in genetically damaged cells. Proapoptotic compounds could also contribute to age-related degenerative diseases by activating cell death in postmitotic cells or shifting the normal balance of mitosis and apoptosis in tissues with regenerative capacity. Many age-related diseases, for example macular degeneration and Parkinson's disease, appear to have oxidative stress as an underlying component that interacts with genetic, dietary, and environmental factors to determine relative risk in an individual. Oxidative stress activates apoptosis, and antioxidants protect against apoptosis in vitro; thus, a central role of dietary antioxidants may be to protect against apoptosis. However, little in vivo data are available to directly link diet with altered apoptosis as an underlying determinant of disease. Moreover, the possible antagonistic effects of different dietary components and the uncertainty about whether proapoptotic compounds that may protect against cancer could contribute to degenerative diseases and vice versa indicate that there is a great need for better in vivo assessment of apoptosis and that caution should be exercised when extrapolating in vitro data on apoptosis to in vivo dietary recommendations.

Original languageEnglish (US)
Pages (from-to)485-505
Number of pages21
JournalAnnual Review of Nutrition
Volume20
DOIs
StatePublished - 2000
Externally publishedYes

Fingerprint

Apoptosis
Diet
Oxidative Stress
Antioxidants
Neoplasms
Macular Degeneration
Mitosis
Uncertainty
Parkinson Disease
Cell Death
Cell Culture Techniques
Health
In Vitro Techniques

Keywords

  • Atherosclerosis
  • Immunity
  • Isoflavones
  • Phase 2 enzyme inducers
  • Zinc

ASJC Scopus subject areas

  • Medicine (miscellaneous)

Cite this

Watson, W. H., Cai, J., & Jones, D. P. (2000). Diet and Apoptosis. Annual Review of Nutrition, 20, 485-505. https://doi.org/10.1146/annurev.nutr.20.1.485

Diet and Apoptosis. / Watson, W. H.; Cai, Jiyang; Jones, D. P.

In: Annual Review of Nutrition, Vol. 20, 2000, p. 485-505.

Research output: Contribution to journalArticle

Watson, WH, Cai, J & Jones, DP 2000, 'Diet and Apoptosis', Annual Review of Nutrition, vol. 20, pp. 485-505. https://doi.org/10.1146/annurev.nutr.20.1.485
Watson, W. H. ; Cai, Jiyang ; Jones, D. P. / Diet and Apoptosis. In: Annual Review of Nutrition. 2000 ; Vol. 20. pp. 485-505.
@article{730822d761ba4ab5912a37bcd006156d,
title = "Diet and Apoptosis",
abstract = "A range of compounds in or derived from the diet modulates apoptosis in cell cultures in vitro. These observations have important implications concerning the mechanisms whereby dietary components affect health. Proapoptotic compounds could protect against cancer by enhancing elimination of initiated, precancerous cells, and antiapoptotic compounds could promote tumor formation by inhibiting apoptosis in genetically damaged cells. Proapoptotic compounds could also contribute to age-related degenerative diseases by activating cell death in postmitotic cells or shifting the normal balance of mitosis and apoptosis in tissues with regenerative capacity. Many age-related diseases, for example macular degeneration and Parkinson's disease, appear to have oxidative stress as an underlying component that interacts with genetic, dietary, and environmental factors to determine relative risk in an individual. Oxidative stress activates apoptosis, and antioxidants protect against apoptosis in vitro; thus, a central role of dietary antioxidants may be to protect against apoptosis. However, little in vivo data are available to directly link diet with altered apoptosis as an underlying determinant of disease. Moreover, the possible antagonistic effects of different dietary components and the uncertainty about whether proapoptotic compounds that may protect against cancer could contribute to degenerative diseases and vice versa indicate that there is a great need for better in vivo assessment of apoptosis and that caution should be exercised when extrapolating in vitro data on apoptosis to in vivo dietary recommendations.",
keywords = "Atherosclerosis, Immunity, Isoflavones, Phase 2 enzyme inducers, Zinc",
author = "Watson, {W. H.} and Jiyang Cai and Jones, {D. P.}",
year = "2000",
doi = "10.1146/annurev.nutr.20.1.485",
language = "English (US)",
volume = "20",
pages = "485--505",
journal = "Annual Review of Nutrition",
issn = "0199-9885",
publisher = "Annual Reviews Inc.",

}

TY - JOUR

T1 - Diet and Apoptosis

AU - Watson, W. H.

AU - Cai, Jiyang

AU - Jones, D. P.

PY - 2000

Y1 - 2000

N2 - A range of compounds in or derived from the diet modulates apoptosis in cell cultures in vitro. These observations have important implications concerning the mechanisms whereby dietary components affect health. Proapoptotic compounds could protect against cancer by enhancing elimination of initiated, precancerous cells, and antiapoptotic compounds could promote tumor formation by inhibiting apoptosis in genetically damaged cells. Proapoptotic compounds could also contribute to age-related degenerative diseases by activating cell death in postmitotic cells or shifting the normal balance of mitosis and apoptosis in tissues with regenerative capacity. Many age-related diseases, for example macular degeneration and Parkinson's disease, appear to have oxidative stress as an underlying component that interacts with genetic, dietary, and environmental factors to determine relative risk in an individual. Oxidative stress activates apoptosis, and antioxidants protect against apoptosis in vitro; thus, a central role of dietary antioxidants may be to protect against apoptosis. However, little in vivo data are available to directly link diet with altered apoptosis as an underlying determinant of disease. Moreover, the possible antagonistic effects of different dietary components and the uncertainty about whether proapoptotic compounds that may protect against cancer could contribute to degenerative diseases and vice versa indicate that there is a great need for better in vivo assessment of apoptosis and that caution should be exercised when extrapolating in vitro data on apoptosis to in vivo dietary recommendations.

AB - A range of compounds in or derived from the diet modulates apoptosis in cell cultures in vitro. These observations have important implications concerning the mechanisms whereby dietary components affect health. Proapoptotic compounds could protect against cancer by enhancing elimination of initiated, precancerous cells, and antiapoptotic compounds could promote tumor formation by inhibiting apoptosis in genetically damaged cells. Proapoptotic compounds could also contribute to age-related degenerative diseases by activating cell death in postmitotic cells or shifting the normal balance of mitosis and apoptosis in tissues with regenerative capacity. Many age-related diseases, for example macular degeneration and Parkinson's disease, appear to have oxidative stress as an underlying component that interacts with genetic, dietary, and environmental factors to determine relative risk in an individual. Oxidative stress activates apoptosis, and antioxidants protect against apoptosis in vitro; thus, a central role of dietary antioxidants may be to protect against apoptosis. However, little in vivo data are available to directly link diet with altered apoptosis as an underlying determinant of disease. Moreover, the possible antagonistic effects of different dietary components and the uncertainty about whether proapoptotic compounds that may protect against cancer could contribute to degenerative diseases and vice versa indicate that there is a great need for better in vivo assessment of apoptosis and that caution should be exercised when extrapolating in vitro data on apoptosis to in vivo dietary recommendations.

KW - Atherosclerosis

KW - Immunity

KW - Isoflavones

KW - Phase 2 enzyme inducers

KW - Zinc

UR - http://www.scopus.com/inward/record.url?scp=0033835866&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033835866&partnerID=8YFLogxK

U2 - 10.1146/annurev.nutr.20.1.485

DO - 10.1146/annurev.nutr.20.1.485

M3 - Article

C2 - 10940343

AN - SCOPUS:0033835866

VL - 20

SP - 485

EP - 505

JO - Annual Review of Nutrition

JF - Annual Review of Nutrition

SN - 0199-9885

ER -