Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Dental & Craniofacial Research (NIDCR)
Type
Research Project (R01)
Project #
5R01DE010873-03
Application #
2131805
Study Section
Oral Biology and Medicine Subcommittee 1 (OBM)
Project Start
1994-02-01
Project End
1999-01-31
Budget Start
1996-02-01
Budget End
1997-01-31
Support Year
3
Fiscal Year
1996
Total Cost
Indirect Cost

  Institution

Name
University of Pennsylvania
Department
Pathology
Type
Schools of Dentistry
DUNS #
042250712
City
Philadelphia
State
PA
Country
United States
Zip Code
19104

  Publications

Shenker, Bruce J; Pankoski, Lisa; Zekavat, Ali et al. (2002) Mercury-induced apoptosis in human lymphocytes: caspase activation is linked to redox status. Antioxid Redox Signal 4:379-89
Shenker, B J; Guo, T L; Shapiro, I M (2000) Mercury-induced apoptosis in human lymphoid cells: evidence that the apoptotic pathway is mercurial species dependent. Environ Res 84:89-99
Close, A H; Guo, T L; Shenker, B J (1999) Activated human T lymphocytes exhibit reduced susceptibility to methylmercury chloride-induced apoptosis. Toxicol Sci 49:68-77
Shenker, B J; Guo, T L; O, I et al. (1999) Induction of apoptosis in human T-cells by methyl mercury: temporal relationship between mitochondrial dysfunction and loss of reductive reserve. Toxicol Appl Pharmacol 157:23-35
Guo, T L; Miller, M A; Shapiro, I M et al. (1998) Mercuric chloride induces apoptosis in human T lymphocytes: evidence of mitochondrial dysfunction. Toxicol Appl Pharmacol 153:250-7
Guo, T L; Miller, M A; Datar, S et al. (1998) Inhibition of poly(ADP-ribose) polymerase rescues human T lymphocytes from methylmercury-induced apoptosis. Toxicol Appl Pharmacol 152:397-405
Shenker, B J; Guo, T L; Shapiro, I M (1998) Low-level methylmercury exposure causes human T-cells to undergo apoptosis: evidence of mitochondrial dysfunction. Environ Res 77:149-59
InSug, O; Datar, S; Koch, C J et al. (1997) Mercuric compounds inhibit human monocyte function by inducing apoptosis: evidence for formation of reactive oxygen species, development of mitochondrial membrane permeability transition and loss of reductive reserve. Toxicology 124:211-24