Radioprotective effect of American ginseng on human lymphocytes at 90 minutes postirradiation: a study of 40 cases.
BACKGROUND
Ionizing radiation (IR) initiates intracellular oxidative stress through enhanced formation of reactive oxygen species (ROS) that attack DNA leading to cell death. Because of the diversity of IR applied in medicine, agriculture, industry, and the growing threats of global terrorism, the acquisition of radioprotectors is an urgent need for the nation. However, the applicability of radioprotectors currently under investigation is limited due to their inherent toxicity.


OBJECTIVE
This study investigated the effect of a standardized North American ginseng extract (NAGE, total ginsenoside content: 11.7%) on DNA damage in human lymphocytes at 90 minutes postirradiation.


METHODS
With the application of NAGE (250-1000 microg mL(-1)) at 90 minutes postirradiation (1 and 2 Gy), DNA damage in lymphocytes obtained from 40 healthy individuals was evaluated by cytokinesis-block micronucleus assay. Similar experiments were also performed in lymphocytes treated with WR-1065 (1 mmol/L or 3 mmol/L). In addition, before and after irradiation, lymphocytes obtained from 10 individuals were measured for their total antioxidant capacity (TAC) and the reactive oxygen species (ROS).


RESULTS
The significant effect of NAGE against (137)Cs-induced micronuclei (MN) in lymphocytes is concentration dependent. NAGE (750 microg mL(-1)) reduced MN yield by 50.7% after 1 Gy and 35.9% after 2 Gy exposures, respectively; these results were comparable to that of WR-1065. Furthermore, we also found that NAGE reduces MN yield and ROS but increases TAC in lymphocytes.


CONCLUSIONS
Our results suggest that NAGE is a relatively nontoxic natural compound that holds radioprotective potential in human lymphocytes even when applied at 90 minutes postirradiation. One of the radioprotective mechanisms may be mediated through the scavenging of free radicals and enhancement of the intracellular TAC.
Lee
Tung-Kwang
TK
Department of Radiation Oncology, Leo W. Jenkins Cancer Center, Brody School of Medicine at East Carolina University, Greenville, NC, USA. leet@ecu.edu
O'Brien
Kevin F
KF
Wang
Weidong
W
Johnke
Roberta M
RM
Sheng
Chao
C
Benhabib
Sidi M
SM
Wang
Tao
T
Allison
Ron R
RR
D000328:Adult; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D004249:DNA Damage; D005260:Female; D036145:Ginsenosides / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D008214:Lymphocytes / Q000187:drug effects* / Q000528:radiation effects; D008297:Male; D008624:Mercaptoethylamines / Q000494:pharmacology; D048629:Micronuclei, Chromosome-Defective; D015162:Micronucleus Tests; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects*; D005894:Panax / Q000737:chemistry*; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use*; D011832:Radiation Injuries / Q000235:genetics / Q000517:prevention & control*; D011839:Radiation, Ionizing; D011837:Radiation-Protective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D017382:Reactive Oxygen Species / Q000378:metabolism; D016037:Single-Blind Method
D000975:Antioxidants; D036145:Ginsenosides; D008624:Mercaptoethylamines; D010936:Plant Extracts; D011837:Radiation-Protective Agents; D017382:Reactive Oxygen Species; C020174:N-(2-mercaptoethyl)-1,3-diaminopropane