In Vivo Radioprotective Effects of Nigella Sativa L Oil and Reduced Glutathione Against Irradiation-Induced Oxidative Injury and Number of Peripheral Blood Lymphocytes in Rats

dc.contributor.author Cemek, Mustafa
dc.contributor.author Enginar, Huseyin
dc.contributor.author Karaca, Turan
dc.contributor.author Unak, Perihan
dc.date.accessioned 2025-05-10T17:07:25Z
dc.date.available 2025-05-10T17:07:25Z
dc.date.issued 2006
dc.description Karaca, Turan/0000-0002-2500-7781 en_US
dc.description.abstract Radiotherapy is one of the most common therapies for treating human cancers. Several studies have indicated that irradiation induces reactive oxygen species (ROS), which play an important role in radiation damage of the cell. It has been shown that Nigella sativa L. (NS) and reduced glutathione (GSH) have both an antiperoxidative effect on different tissues and a scavenger effect on ROS. The purpose of this study was to determine the antioxidant and radioprotective roles of INS and GSH against irradiation-induced oxidative injury in an experimental model. The INS group was administrated INS (1 mL/kg body weight), the GSH group was injected GSH (150 mg/kg body weight) and the control group was given physiologic saline solution (1 mL/kg body weight) for 30 consecutive days before exposure to a single dose of 6 Gy of radiation. Animals were sacrificed after irradiation. Malondialdehyde, nitrate, nitrite (oxidative stress markers) and ascorbic acid, retinol, beta-carotene, GSH and ceruloplasmin (nonenzymatic antioxidant markers) levels and peripheral blood lymphocytes were measured in all groups. There were statistically significant differences between the groups for all parameters (P < 0.05). Whole-body irradiation caused a significant increase in blood malondial-dehyde, nitrate and nitrite levels. The blood oxidative stress marker levels in irradiated rats that were pretreated with NS and GSH were significantly decreased; however, nonenzymatic antioxidant levels were significantly increased. Also, our results suggest that NS and GSH administration prior to irradiation prevent the number of alpha-naphthyl acetate esterase peripheral blood T lymphocytes from declining. These results clearly show that NS and GSH treatment significantly antagonize the effects of radiation. Therefore, NS and GSH may be a beneficial agent in protection against ionizing radiation-related tissue injury. en_US
dc.identifier.doi 10.1562/2006-06-15-RA-924
dc.identifier.issn 0031-8655
dc.identifier.issn 1751-1097
dc.identifier.scopus 2-s2.0-33846546568
dc.identifier.uri https://doi.org/10.1562/2006-06-15-RA-924
dc.identifier.uri https://hdl.handle.net/20.500.14720/6762
dc.language.iso en en_US
dc.publisher Wiley-blackwell en_US
dc.rights info:eu-repo/semantics/closedAccess en_US
dc.title In Vivo Radioprotective Effects of Nigella Sativa L Oil and Reduced Glutathione Against Irradiation-Induced Oxidative Injury and Number of Peripheral Blood Lymphocytes in Rats en_US
dc.type Article en_US
dspace.entity.type Publication
gdc.author.id Karaca, Turan/0000-0002-2500-7781
gdc.author.scopusid 6602477797
gdc.author.scopusid 56190302200
gdc.author.scopusid 22985194700
gdc.author.scopusid 7003859320
gdc.author.wosid Karaca, Turan/Abd-6669-2020
gdc.author.wosid Ünak, Perihan/Aay-3145-2020
gdc.coar.access metadata only access
gdc.coar.type text::journal::journal article
gdc.description.department T.C. Van Yüzüncü Yıl Üniversitesi en_US
gdc.description.departmenttemp Afyon Kocatepe Univ, Fac Sci & Arts, Dept Chem, Div Biochem, Afyon, Turkey; Afyon Kocatepe Univ, Fac Sci & Arts, Dept Chem, Afyon, Turkey; Yuzuncu Yil Univ, Fac Med Vet, Dept Histol Embryol, Van, Turkey; Ege Univ, Inst Sci Nucl, Dept Nucl Applicat, Bornova, Turkey en_US
gdc.description.endpage 1696 en_US
gdc.description.issue 6 en_US
gdc.description.publicationcategory Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı en_US
gdc.description.scopusquality Q2
gdc.description.startpage 1691 en_US
gdc.description.volume 82 en_US
gdc.description.woscitationindex Science Citation Index Expanded
gdc.description.wosquality Q2
gdc.identifier.pmid 17387769
gdc.identifier.wos WOS:000243214100044
gdc.index.type WoS
gdc.index.type Scopus
gdc.index.type PubMed

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