Akademik Veri Yönetim Sistemi
The 16th European Microscopy Congress, Lyon, Fransa, 28 Ağustos - 02 Eylül 2016, ss.6179
Diabetes is a chronic metabolic disease which lasts for the whole life. Cancer is the second cause of death in the
world, according to World Health Organization data. Association of diabetes with cancer is a major health
concern. Diabetes and cancer is a serious metabolic disorder with many functional and structural complications
as well as having a significant impact both directly and indirectly on all systems (1). Prostate cancer has a great
importance for male morbidity and mortality observed both in our country and also in the globe. It is at the
second rank among cancer-related mortality cases. Prostate cancer can be determined as the alteration of the
balance between cell proliferation and cell death in the prostate which causes a malign increase of the organ
volume. Dunning prostate cancer model is formed by subcutaneous injection of strongly metastatic MAT-Lylu
cells in a Copenhagen rats (2). Experimental diabetes model is widely induced by streptozotocin (STZ).
Metformin is a drug that used for the treatment of type 2 diabetes. Besides, the studies related to reduce the risk
of cancer of the metformin have recently drawn attention (3). The aim of this study is to investigate the role of
metformin on testicular damage in diabetic+prostate cancer model.
Male Copenhagen rats were divided into three groups: 1) Control group: % 0.9 physiological saline was received
during 14 days, 2) Diabetic+ cancer group: 2x104
Mat-LyLu cells were received after injection of 65 mg/kg STZ.
3) Diabetic+ cancer+metformin group: metformin was received 250 mg/kg during experimental period,
following injection of STZ and inocculation of Mat-LyLu cells. At the end of the experimental period (day 14)
testes tissues were taken. Tissues were stained with hematoxylin and eosin and periodic acid-Schiff reaction and
determined the degree of histopathological damage. The degree of histopathological damage in the seminiferous
tubules were evaluated as: normal, regressive, degenerative and atrophic (4). Apoptotic cells in testes tissue
were detected with TUNEL reaction. Biochemically, serum glucose, glutathione, malondialdehyde, prostate
specific antigen levels and testis protein carbonyl levels and myeloperoxidase, xanthine oxidase activities were
determined.
Testes tissue of the control group presented a normal testicular morphology and regular seminiferous tubules.
The histopathological damage score of testicular tissue was significantly increased in diabetic+cancer group
compared to control group. The number of regressive and degenerative tubules in diabetic+cancer+metformin
group was decreased by metformin treatment. TUNEL positive cells were observed in all groups. The total
number of TUNEL positive cells throughout the testes was increased in diabetic+cancer+metformin group
compared to diabetic+cancer group. According to biochemical data, serum glutathione levels were decreased in
diabetic+cancer group compared to control group. Serum glucose, malondialdehyde, prostate specific antigen
levels, and testis protein carbonyl levels and myeloperoxidase and xanthine oxidase activities were increased in
diabetic+cancer group. Treatment with metformin reversed these effects.
It was indicated that metformin has been shown to be protective against testicular damage in diabetic male rats
(5). It was has been reported that metformin was used as protective agent to prevent high-fat diet induced
testicular damage. Metformin inhibits the growth of cancer cell lines which suggests that it also has an
inhibitory effect on cancer progression (6,7). Our results suggest that administration of metformin prevents the
testicular damage by ameliorating the oxidative stress parameters and tissue damage. In conclusion, we can say
that metformin has a potential protective effect on the testes tissue in diabetes and Dunning prostate cancer
model.