The effect of intratympanic oxytocin treatment on rats exposed to acoustic trauma.

OBJECTIVE: To investigate whether oxytocin can prevent ototoxicity related to acoustic trauma. METHODS: Twenty-eight rats were divided into four groups: noise (group 1), control (group 2), noise plus oxytocin (group 3), and oxytocin (group 4). Intratympanic oxytocin was administered on days 1, 2, 4, 6, 8 and 10 in groups 3 and 4. Groups 1 and 3 were exposed to acoustic trauma. Distortion product otoacoustic emission and auditory brainstem response testing were performed in all groups. RESULTS: In group 1, auditory brainstem response thresholds increased significantly after acoustic trauma. In group 3, auditory brainstem response thresholds increased significantly on day 1 after acoustic trauma, but there were no significant differences between thresholds at baseline and on the 7th and 21st days. In group 1, significant differences were observed between distortion product otoacoustic emission signal-to-noise ratios measured before and on days 1, 7 and 21 after acoustic trauma. In group 3, no significant differences were observed between the distortion product otoacoustic emission signal-to-noise ratios measured before and on days 7 and 21 after acoustic trauma. CONCLUSION: Oxytocin had a therapeutic effect on rats exposed to acoustic trauma in this experiment.

Comparison of the protective effects of intratympanic dexamethasone and methylprednisolone against cisplatin-induced ototoxicity.

OBJECTIVE: This study aimed to compare the efficacies of intratympanic dexamethasone and methylprednisolone in preventing in cisplatin-induced ototoxicity in rats. METHODS: Experimental groups of rats (n = 8 each) received intratympanic isotonic saline, intraperitoneal cisplatin and intratympanic isotonic saline, intraperitoneal cisplatin and intratympanic dexamethasone, or intraperitoneal cisplatin and intratympanic methylprednisolone. Distortion product otoacoustic emission thresholds were compared on days 0 and 10 in all rats, and correlations between drug effects and changes in cochlear histology were evaluated. RESULTS: Distortion product otoacoustic emission thresholds were comparable in groups III and IV (p > 0.05). Significant protection against cisplatin-induced ototoxicity was seen in groups III and IV compared with group II (p < 0.05). Dexamethasone and, to a lesser extent, methylprednisolone protected against cellular apoptosis in cisplatin-induced ototoxicity. CONCLUSION: Dexamethasone (and possibly methylprednisolone) may be clinically useful as an intratympanic chemopreventive agent to treat cisplatin ototoxicity. Future clinical studies should investigate the use of dexamethasone for this purpose in adult patients.

Antifibrogenic role of valproic acid in streptozotocin induced diabetic rat penis.

We investigated the therapeutic effects of valproic acid (VPA) on erectile dysfunction and reducing penile fibrosis in streptozocin (STZ)-induced diabetic rats. Eighteen male rats were divided into three experimental groups (Control, STZ-DM, STZ-DM plus VPA) and diabetes was induced by transperitoneal single dose STZ. Eight weeks after, VPA and placebo treatments were given according to groups for 15 days. All rats were anesthetised for the measurement of in vivo erectile response to cavernous nerve stimulation. Afterward penes were evaluated histologically in terms of immune labelling scores of endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF) and transforming growth factor-ß1 (TGF-ß1). Slides were also evaluated in terms of collagen/smooth muscle ratio and penile apoptosis. After the treatment with VPA, erectile responses were found as improved when compared with STZ-DM rats but not statistically meaningful. eNOS and VEGF immune expressions diminished in penile corpora of STZ-DM rats and improved with VPA treatment. VPA led to decrease in TGF-ß1 expression and collagen content of diabetic rats' penes. Penile apoptosis was not diminished with VPA. In conclusion, VPA treatment seems to be effective for reducing penile fibrosis in diabetic rats and more prolonged treatment period may enhance erectile functions.

Usage of whey protein may cause liver damage via inflammatory and apoptotic responses.

The purpose of this study was to investigate the long- and short-term inflammatory and apoptotic effects of whey protein on the livers of non-exercising rats. Thirty rats were divided into three groups namely (1) control group, (2) short-term whey (WS) protein diet (252 g/kg for 5 days), and (3) long-term whey (WL) protein diet (252 g/kg for 4 weeks). Interleukin 1ß (IL-1ß), IL-6, tumor necrosis factor α (TNF-α), and cytokeratin 18 (CK-18-M30) were assessed using enzyme-linked immunosorbent assay and immunohistochemical methods. Apoptosis was evaluated using the terminal transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) method. Hepatotoxicity was evaluated by quantitation of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Based on the biochemical levels and immunohistochemical results, the highest level of IL-1ß was identified in the WL group (p < 0.01). The IL-6 and TNF-α results were slightly lower in the WS group than in the control group and were highest in the WL group (p < 0.01). The CK-18-M30 and TUNEL results were highest in the WS group and exhibited medium intensity in the WL group (p < 0.01). AST results were statistically significant for all groups, while our ALT groups were particularly significant between the WL and control groups (p < 0.01). The results showed that when whey protein is used in an uninformed manner and without exercising, adverse effects on the liver may occur by increasing the apoptotic signal in the short term and increasing inflammatory markers and hepatotoxicity in the long term.

The effect of histamine on kidney by fasting in rats.

BACKGROUND: The aim of this study was to investigate ultrastructural and apoptotic changes occurring in the kidneys in fasting individuals and to examine the effects of histamine treatment at the electron-microscopic and immunohistochemical levels. METHODS: Eighteen adult Wistar male rats were randomly divided into three groups (n=6 for each). Control group (1), fasting group (12 h) (2), and fasting+histamine injection (0.5 mg/kg) (3) group. Expression of caspase-3 and caspase-9 was determined in the tissue sections using immunohistochemical techniques. Quantitative data were obtained using H-SCORE, and statistical evaluations were then performed. The ultrastructure of the kidney tissues was examined using transmission electron microscopy. RESULTS: Weak caspase-3 and caspase-9 expression was observed in the renal tubules and glomeruli in the control group, while immunoreactivity was more intense in the fasting group (p<0.05). In the fasting+histamine group, caspase-3 and caspase-9 immunostaining was significantly positive in both renal tubules and glomeruli (p<0.05). At electron microscopic evaluation, degenerative changes were seen in the glomeruli of the fasting group, as well as partial vacuolization and disruption at the basal foldings in the tubular epithelial cells. In the fasting+histamine group, in addition to significant dilatation of all glomerular capillaries, there were degenerative changes in all tubular and canalicular epithelial cells in the proximal tubules. CONCLUSIONS: Fasting, an important metabolic stress factor, accompanied by histamine treatment may cause significant disruptions in the kidneys, particularly in the glomerular capillaries and proximal and distal tubules (Tab. 1, Fig. 2, Ref. 34).