Role of acetyl-CoA acetyltransferase 1 expression in the molecular mechanism of adenomyosis.

Objective: Adenomyosis is a benign uterine illness characterized by endometrial gland and stromal invasion into the myometrium. Acetyl-CoA acetyltransferase 1 (ACAT1) is an enzyme localized in mitochondria that is involved in ketogenesis and ketolysis processes by reversibly catalyzing the formation of acetoacetyl-CoA from two acetyl-CoA molecules. The current study investigated the expression of the ACAT1 molecule in tissue samples of patients diagnosed with adenomyosis and healthy endometrial tissues. It is aimed to determine the differences in ACAT1 gene expression and in this way to discover the first information about the role of ACAT1 in the development and molecular mechanism of adenomyosis. Materials and Methods: In the current retrospective study, formalin-fixed paraffin-embedded archival tissues were employed. A total of 76 patient samples were included in the study. Of these samples, 28 are adenomyotic tissue (Group I), 30 are eutopic endometrial tissue (Group II), and 18 are the Control Group. In these groups, the expression levels of the ACAT1 gene were determined by the reverse transcription-polymerase chain reaction method. Results: When the expression results of the ACAT1 gene were evaluated, statistically significant differences were found between the groups (p<0.05). There was a difference between Group I-Group II and Group I-Control Group regarding the ACAT1 gene. No statistically significant change was observed between Group II and Control Group. It is a remarkable finding that the expression of ACAT1 in adenomyosis tissue is decreased compared with both eutopic endometrium and control groups tissues. Conclusion: The results suggest that ACAT1 may be associated with the molecular pathogenesis of adenomyosis.

Affirmative effects of iloprost on apoptosis during ischemia-reperfusion injury in kidney as a distant organ.

OBJECTIVE: Apoptosis and its regulatory mechanisms take part in renal ischemia-reperfusion (I/R) injury which can result in acute renal failure and the inhibition of the caspase is considered as a new therapeutic strategy. In this context, we investigated the antiapoptotic and cytoprotective effects of iloprost, a prostacyclin analog, in kidney as a distant organ. METHODS: Wistar albino rats were randomized into five groups (n = 12 in each) as sham, ischemia, I/R, iloprost (10 µg kg(-1)), and I/R + iloprost (10 µg kg(-1)). A 4 h reperfusion procedure was carried out after 4 h of ischemia. Caspase-8 was evaluated for death receptor-induced pathways, whereas caspase-9 was evaluated for mitochondria-dependent pathways and caspase-3 was investigated for overall apoptosis. Superoxide dismutase (SOD) enzyme activity and nitrite content as an indicator of nitric oxide (NO) production were also analyzed in kidney tissues. RESULTS: Caspases-3, -8, and -9 were all significantly elevated in both ischemia and I/R groups compared to the sham group; however, treatment with iloprost reduced caspases-3, -8, and -9. SOD enzyme activity was attenuated by iloprost when compared to ischemic rats. The different effects of NO were found which change according to the present situation in ischemia, I/R, and treatment with iloprost. CONCLUSIONS: These findings suggested that iloprost prevents apoptosis in both receptor-induced and mitochondria-dependent pathways in renal I/R injury and it may be considered as a cytoprotective agent for apoptosis. Understanding the efficiency of iloprost on the pathways for cell death may lead to an opportunity in the therapeutic approach for renal I/R injury.

The effect of human growth hormone on superoxide dismutase activity, glutathione and malondialdehyde levels of hypoxic-ischemic newborn rat brain.

OBJECTIVES: We investigated the effect of human growth hormone (GH) on newborn rat brain superoxide dismutase, glutathione and malondialdehyde (MDA) levels in hypoxic-ischemic (H-I) newborn rats. METHODS: Fourty-eight 7 days old newborn rats were randomized to a healthy (n: 15), H-I (n: 18) and GH administered H-I (GH-H-I, n: 15) group. Permanent, left common carotid ligation was performed in the H-I groups. In the GH-H-I group, 50 mg/kg human GH (Norditropin Simplex, Novo Nordisk A/S) was administered subcutaneously just before carotid artery ligation. Two hours after ligation, rats were subjected to 2 h of hypoxemia and then were decapitated. Right and left cerebral hemispheres (CHs) and cerebellum-brain stem (C-BS) were separated. RESULTS: Glutathione levels of each region were not statistically different from each other in and between the groups. Superoxide dismutase levels were higher in C-BSs compared to CHs (for each comparison p < 0.01). CHs and C-BS MDA levels were similar in the control and H-I groups but MDA levels of both CHs of the GH-H-I group were significantly higher than the levels of the H-I group (p = 0.01; p = 0.024, respectively). Left CH MDA level of GH-H-I group was higher compared to left CH MDA of the control group (p = 0.045) while there was no difference between right CHs. In the GH-H-I group, left CH MDA level was higher than the C-BS (p = 0.03). MDA levels of the C-BSs did not differ between the groups (p > 0.05). CONCLUSION: Although we have not evaluated the effect of GH histopathologically, increased lipid peroxidation especially in the H-I (left) hemisphere of the GH treated rats might suggest that GH treatment may be harmful in H-I encephalopathy.