Tags

Type your tag names separated by a space and hit enter

Smokeless tobacco, oxidative stress, apoptosis, and antioxidants in human oral keratinocytes.
Free Radic Biol Med. 1999 Apr; 26(7-8):992-1000.FR

Abstract

We have investigated the effects of a smokeless tobacco extract (STE) on lipid peroxidation, cytochrome c reduction, DNA fragmentation and apoptotic cell death in normal human oral keratinocyte cells, and assessed the protective abilities of selected antioxidants. The cells, isolated and cultured from human oral tissues, were treated with STE (0-300 microl;g/ml) for 24 h. Superoxide anion production was determined by cytochrome c reductase. Oxidative tissue damage was determined by lipid peroxidation and DNA fragmentation, whereas apoptotic cell death was assessed by flow cytometry. STE-induced fragmentation of genomic DNA was also determined by gel electrophoresis. The comparative protective abilities of vitamin C (75 microM), vitamin E (75 microM), a combination of vitamins C & E (75 microM each), and a novel grape seed proanthocyanidin (IH636) extract (GSPE) (100 microg/ml) against STE induced oxidative stress and tissue damage were also determined. Following treatment of the cells with 300 microg STE/ml 1.5-7.6-fold increases in lipid peroxidation, cytochrome c reduction and DNA fragmentation were observed. The addition of the antioxidants to cells treated with STE provided 10-54% decreases in these parameters. Approximately 9, 29, and 35% increases in apoptotic cell death were observed following treatment with 100, 200, and 300 microg STE/ml, respectively, and 51-85% decreases in apoptotic cell death were observed with the antioxidants. The results demonstrate that STE produces oxidative tissue damage and apoptosis, which can be attenuated by antioxidants including vitamin C, vitamin E, a combination of vitamins C plus E and GSPE. GSPE exhibited better protection against STE than vitamins C and E, singly and in combination.

Authors+Show Affiliations

Creighton University School of Pharmacy and Allied Health Professions, Omaha, NE, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10232844

Citation

Bagchi, M, et al. "Smokeless Tobacco, Oxidative Stress, Apoptosis, and Antioxidants in Human Oral Keratinocytes." Free Radical Biology & Medicine, vol. 26, no. 7-8, 1999, pp. 992-1000.
Bagchi M, Balmoori J, Bagchi D, et al. Smokeless tobacco, oxidative stress, apoptosis, and antioxidants in human oral keratinocytes. Free Radic Biol Med. 1999;26(7-8):992-1000.
Bagchi, M., Balmoori, J., Bagchi, D., Ray, S. D., Kuszynski, C., & Stohs, S. J. (1999). Smokeless tobacco, oxidative stress, apoptosis, and antioxidants in human oral keratinocytes. Free Radical Biology & Medicine, 26(7-8), 992-1000.
Bagchi M, et al. Smokeless Tobacco, Oxidative Stress, Apoptosis, and Antioxidants in Human Oral Keratinocytes. Free Radic Biol Med. 1999;26(7-8):992-1000. PubMed PMID: 10232844.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Smokeless tobacco, oxidative stress, apoptosis, and antioxidants in human oral keratinocytes. AU - Bagchi,M, AU - Balmoori,J, AU - Bagchi,D, AU - Ray,S D, AU - Kuszynski,C, AU - Stohs,S J, PY - 1999/5/8/pubmed PY - 1999/5/8/medline PY - 1999/5/8/entrez SP - 992 EP - 1000 JF - Free radical biology & medicine JO - Free Radic Biol Med VL - 26 IS - 7-8 N2 - We have investigated the effects of a smokeless tobacco extract (STE) on lipid peroxidation, cytochrome c reduction, DNA fragmentation and apoptotic cell death in normal human oral keratinocyte cells, and assessed the protective abilities of selected antioxidants. The cells, isolated and cultured from human oral tissues, were treated with STE (0-300 microl;g/ml) for 24 h. Superoxide anion production was determined by cytochrome c reductase. Oxidative tissue damage was determined by lipid peroxidation and DNA fragmentation, whereas apoptotic cell death was assessed by flow cytometry. STE-induced fragmentation of genomic DNA was also determined by gel electrophoresis. The comparative protective abilities of vitamin C (75 microM), vitamin E (75 microM), a combination of vitamins C & E (75 microM each), and a novel grape seed proanthocyanidin (IH636) extract (GSPE) (100 microg/ml) against STE induced oxidative stress and tissue damage were also determined. Following treatment of the cells with 300 microg STE/ml 1.5-7.6-fold increases in lipid peroxidation, cytochrome c reduction and DNA fragmentation were observed. The addition of the antioxidants to cells treated with STE provided 10-54% decreases in these parameters. Approximately 9, 29, and 35% increases in apoptotic cell death were observed following treatment with 100, 200, and 300 microg STE/ml, respectively, and 51-85% decreases in apoptotic cell death were observed with the antioxidants. The results demonstrate that STE produces oxidative tissue damage and apoptosis, which can be attenuated by antioxidants including vitamin C, vitamin E, a combination of vitamins C plus E and GSPE. GSPE exhibited better protection against STE than vitamins C and E, singly and in combination. SN - 0891-5849 UR - https://www.unboundmedicine.com/medline/citation/10232844/Smokeless_tobacco_oxidative_stress_apoptosis_and_antioxidants_in_human_oral_keratinocytes_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0891-5849(98)00286-X DB - PRIME DP - Unbound Medicine ER -