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Protective effects of fish omega‐3 fatty acids on doxorubicin‐induced testicular apoptosis and oxidative damage in rats
Author(s) -
Uygur R.,
Aktas C.,
Tulubas F.,
Uygur E.,
Kanter M.,
Erboga M.,
Caglar V.,
Topcu B.,
Ozen O. A.
Publication year - 2014
Publication title -
andrologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.633
H-Index - 59
eISSN - 1439-0272
pISSN - 0303-4569
DOI - 10.1111/and.12173
Subject(s) - malondialdehyde , glutathione peroxidase , glutathione , apoptosis , oxidative stress , superoxide dismutase , polyunsaturated fatty acid , terminal deoxynucleotidyl transferase , doxorubicin , chemistry , fish oil , pharmacology , fatty acid , biochemistry , biology , andrology , tunel assay , medicine , fish <actinopterygii> , chemotherapy , enzyme , fishery
Summary The aim of this study was to examine the protective effects of fish omega‐3 (n‐3) fatty acids on acute doxorubicin ( DOX )‐induced testicular apoptosis and oxidative damage. 24 male rats were divided into three groups: control, DOX ‐treated and DOX +fish n‐3 fatty acids. Fish n‐3 fatty acids (400 mg kg −1 ) were given for 30 days by intragastric gavage. The rats received a single intraperitoneal injection of DOX (30 mg kg −1 ) and were sacrificed after 48 h. The DOX +fish n‐3 fatty acids group showed a decrease in malondialdehyde levels and increased activities of superoxide dismutase and glutathione peroxidase in comparison with the DOX ‐treated group. Acute DOX treatment caused severe damage such as disorganisation and separation of germ cells. The fish n‐3 fatty acids‐pretreated rats showed an improved histological appearance in the DOX ‐treated group. Our data indicate a reduction in the activity of terminal deoxynucleotidyl transferase mediated dUTP nick end labelling; there was a rise in the expression of proliferating cell nuclear antigen in testis tissues of the DOX +fish n‐3 fatty acids group compared with DOX ‐treated group. These data suggested that fish n‐3 fatty acids pre‐treatment may be beneficial for spermatogenesis following acute DOX ‐induced testicular damage by decreasing germ cell apoptosis and oxidative stress.

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