Therapeutic role of boron on acrylamide-induced nephrotoxicity, cardiotoxicity, neurotoxicity, and testicular toxicity in rats: Effects on Nrf2/Keap-1 signaling pathway and oxidative stress.

BACKGROUND: Acrylamide (ACR) is a heat-related carcinogen used in cooking some foods as well as in other thermal treatments. The present study aims to investigate the possible protective effect of boron (BA) against ACR-induced toxicity of kidney, brain, heart, testis, and bladder tissues in rats. METHODS: Rats have been divided into 5 equal groups: Control (saline), ACR (38.27 mg/kg), BA (20 mg/kg), BA+ ACR (10 mg/kg + ACR), and BA+ ACR (20 mg/kg BA+ACR). Kidney tissue from rats was collected and the levels of malondialdehyde (MDA), glutathione (GSH), and the activity of superoxide dismutase (SOD) were measured. In addition, the kidneys of these animals, as well as the brain, heart, testes, and bladder tissues were examined for possible histological changes. Total Nrf2 and Keap-1 protein expression in kidney, heart, and testis tissues was examined by immunohistochemistry. RESULTS: While significant increases in MDA levels were observed in the kidneys of rats receiving ACR alone, significant decreases in antioxidant markers (SOD and GSH) were observed. Besides, kidney, brain, heart, and testicular tissues were analyzed and damage was observed in the groups receiving ACR. However, no significant histologic changes were noted in the bladder tissue. Both dosages of BA in combination with ACR improved the changes in ACR-induced antioxidant tissue parameters. Despite the fact that MDA levels were decreased with these two dosages, histological structural abnormalities were found to be greatly improved. CONCLUSION: Our results show that BA has a strong protective effect on ACR-induced multi-organ toxicity. The study results show that BA could be a potential element to reduce ACR toxicity to which we are often exposed.

Mode of onset of polymorphic ventricular tachycardia in acute myocardial infarction.

BACKGROUND: Polymorphic ventricular tachycardia (PVT) can occur during acute myocardial infarction (MI). In the past, studies investigated the initiation pattern of ventricular tachycardias in different patient populations; however, the mode of onset of PVT in acute MI patients has not been investigated previously. OBJECTIVE: To retrospectively investigate the electrophysiological features of PVT with different initiation patterns in acute MI patients to assess whether there is a relationship of the initiation patterns of PVT with clinical and electrophysiological characteristics. METHODS: Sixty-two rhythm strips defined as PVT from 53 patients (mean [± SD] age 63±8 years) with acute ST elevation MI were analyzed. All patients were monitored while they were hospitalized in the coronary care unit, and the electrocardiogram strips were obtained from continuous monitoring. PVT was defined as sudden-onset tachycardia if it was not preceded by ventricular ectopic beats. PVT that was preceded by single or multiple ectopic beats was defined as nonsudden-onset tachycardia. RESULTS: Nonsudden-onset episodes were more common than suddenonset episodes (40 episodes [64.5%] versus 22 episodes [35.5%]). In the nonsudden-onset group, 25 episodes (62.5%) were initiated after a single ectopic beat, while 15 episodes (37.5%) were initiated after multiple complexes. The mean (± SD) left ventricular ejection fraction of patients with nonsudden-onset PVT was decreased (53±6% versus 65±7%, P<0.01). Nonsudden-onset tachycardias had lower coupling intervals than suddenonset tachycardias. Similarly, the PVT cycle length was shorter in the presence of nonsudden-onset initiation. When nonsudden-onset PVT episodes were further subclassified based on the morphology of the first beat of tachycardia, 26 PVTs (65%) had a first beat of tachycardia similar to the subsequent PVT beats and 14 (35%) did not. CONCLUSIONS: These results demonstrate that PVT is often preceded by ventricular ectopy in acute MI patients. Nonsudden-onset PVT is usually characterized by a lower coupling interval, shorter PVT cycle length and an associated lower ejection fraction.

Metastasis from breast carcinoma to a tamoxifen-related endometrial polyp.

BACKGROUND: Metastasis of extragenital neoplasms to an endometrial polyp is rare and until now, only 6 cases of such involvement has been described. CASE: A 58-year-old woman, who had been diagnosed 4 years ago with infiltrating ductal breast carcinoma and treated with surgery and tamoxifen therapy, was admitted to the gynecology clinic because of endometrial thickening observed during a routine abdominal ultrasonographic examination. A total hysterectomy with bilateral salpingo-oophorectomy was performed. Pathological examination of the specimen showed a large polyp which microscopically showed clusters of cells with signet ring morphology within the polyp stroma. The positivity of tumor cells for GCDFP-15 supported the diagnosis of metastatic breast carcinoma to endometrial polyp. CONCLUSION: Metastatic breast carcinoma should be considered in the differential diagnosis of carcinomas with signet ring cell morphology involving uterus.