The Effects of Lung Ischaemia/Reperfusion on TRPM Gene Expression

ABSTRACT Objective: Transient receptor potential melastatin (TRPM) are integral membrane proteins that have broad range of cellular functions. Roles of TRPM2, TRPM3, TRPM4 and TRPM7 among these channels are very important, and their roles in lung ischaemia/reperfusion injury have not been evaluated yet. The aim of this study is to investigate the contribution of these genes in lung ischaemia/reperfusion injury and evaluate histopathology of tissues. Methods: A total of 40 Wistar albino rats were enrolled for the study. Ischaemia was performed by the application of an atramvatic clamp to pulmonary artery. Gene expressions were determined by the semi-quantitative reverse transcription-polymerase chain reaction method. Histopatholical evaluations were held by a standard haematoxyline-eosin staining. Results: The major histopathological tissue damage was observed in ischaemia performed groups, and expression of TRPM channels was found to be obviously downregulated. Substantial changes were determined between TRPM2, TRPM3, TRPM4 and TRPM7 and lung ischaemia/reperfusion injury. In particular, expression of TRPM2 and TRPM7 was reversibly downregulated in ischaemia. Yet, the expression of TRPM3 and TRPM4 was irreversibly down-regulated after ischaemia. Conclusion: Consequently, these results indicate that TRPM family of cation channels may have significant roles in the lung ischaemia/reperfusion injury.

Effects of whole-body hypoxic preconditioning on hypoxia/reoxygenation-induced intestinal injury in newborn rats.

PURPOSE: The precise cause of necrotizing enterocolitis (NEC) is elusive. Ischemia and reperfusion injury of the intestine has been considered to be a major contributing factor for NEC. Ischemic preconditioning is defined as one or more brief periods of ischemia with intermittent reperfusion that protects tissues against a sustained period of subsequent ischemia. Contribution of preconditioning to hypoxia/reoxygenation-induced intestinal injury in newborn rats has not been evaluated previously. METHODS: The study was carried out on 1-day-old Wistar albino rat pups. Whole-body hypoxia and reoxygenation (H/R) was achieved by 10 min hypoxia using 95 % N (2) + 5 % CO (2) followed by 10 min reoxygenation with 100 % oxygen. Whole body hypoxic preconditioning (HP) cycles were performed with 3 min hypoxia and 5 min reoxygenation. Thirty-three pups were randomly allocated into 4 groups. Group 1 served as untreated controls. The pups in group 2 were subjected to H/R only. In groups 3 and 4, 1 cycle and 3 cycles of HP were performed prior to H/R, respectively. Animals were killed at the end of the protocols. Intestine specimens were obtained to determine the histological changes, as well as to measure the tissue malondialdehyde (MDA) and nitric oxide (NO) levels, and xanthine oxidase (XO) and myeloperoxidase (MPO) activities. RESULTS: The microscopic lesions in H/R rat pups were virtually the same as those seen in neonatal NEC, with severe destruction of villi and crypts, in some cases extending to the muscularis. In both HP groups, the lesions were found to be milder. H/R resulted in a marked elevation in MDA and NO levels, and XO and MPO activities compared to the untreated controls. Both 1 cycle and 3 cycles of HP prior to H/R resulted in an obvious decrease in all biochemical parameters. Differences of the biochemical results between both HP groups were not statistically significant. CONCLUSION: This study revealed that whole-body hypoxic preconditioning is beneficial for hypoxia/reoxygenation-induced intestinal injury in newborn rats.

The electrocardiogram of the Pekin duck.

In this study, standard limb lead electrocardiograms (ECG) were recorded in 50 Pekin ducks. The ECG exhibited P, R, S, and T waves. A Q wave was observed in 30% of leads aVR aVL. All waves in lead I were of very low amplitude or almost isoelectric. The P wave was 20% negative, 80% positive in lead aVR and always positive in other leads. The duration and amplitude of P wave were 0.025 sec and 0.17 mV, respectively, and the P-R interval was 0.06 sec in lead II. A Q wave was observed in 30% of leads aVR and aVL but was invisible in other leads. The duration of QRS complex was 0.036 sec and its amplitude was 0.069 mV. The S wave (rS) was greater than the R wave in leads III and aVF. The R and S waves were equal in lead III (66%). The mean duration and amplitude of T wave were 0.05 sec and 0.22 mV, respectively. The T wave was negative in leads aVR and aVL and positive in other leads. The Q-T interval was 0.10 sec. The mean heart rate was 281.3 (220-375) beats/min. The average value of the mean electrical axis was +147 degrees (+95 degrees to -160 degrees).

Effect of verapamil and lidocaine on TRPM and NaV1.9 gene expressions in renal ischemia-reperfusion.

BACKGROUND: To determine effects on calcium and sodium channels of Ca(2+) and Na(+) channel blockers in the present study, expression levels of TRPM1, TRPM2, TRPM3, TRPM4, TRPM5, TRPM6, TRPM7, TRPM8, and NaV1.9 genes were evaluated in kidney tissues after induced ischemia-reperfusion. MATERIAL AND METHODS: Forty albino Wistar male rats were equally divided into 4 groups as follows: group I: control group (n = 10), group II: ischemia group (60 minutes of ischemia + 48 hours of reperfusion; n = 10), group III: ischemia (60 minutes of ischemia + 48 hours of reperfusion) + calcium channel blocker (n = 8), group IV: ischemia (60 minutes of ischemia + 48 hours of reperfusion) + sodium channel blocker (n = 8). RESULTS: When compared to ischemia group expression levels of TRPM2, TRPM4, TRPM6, and NaV1.9 in Ca(2+) and Na(+) channel blocker groups were increased, whereas that of TRPM7 was decreased. However, expression levels of TRPM1, TRPM3, TRPM5, and TRPM8 were not determined in kidney tissue. Histologically, the Ca(2+) channel blocker verapamil and the Na(+) channel blocker lidocaine inhibited the cell death in kidney tissue compared to control. CONCLUSION: Our study suggested that verapamil and lidocaine significantly reduce the degree of ischemia-reperfusion injury due to effects to TRPM and Nav1.9 genes.

Occupational lead exposure effect on liver functions and biochemical parameters.

The effect of occupational lead exposure on the liver function and on the blood biochemical parameters among the battery workers and the muffler repair workers was studied. The study included 22 battery and 38 muffler repair workers. Whole blood lead levels were determined by atomic absorption spectrophotometers. Total protein, albumin, globulin, cholesterol, triglyceride, total bilirubin, aspartate transaminase (AST), alanine transaminase (ALT), gamma glutamyltransferase (GGT), lactate dehydrogenase (LDH), and alkaline phosphatase (ALP) levels were determined in the serum by spectrophotometry. The blood lead levels of the battery workers, muffler repair workers, and the controls were found to be 36.83 +/- 8.13 microg/dL, 26.99 +/- 9.42 microg/dL, and 14.81 +/- 3.01 microg/dL, respectively. Blood lead levels of the workers were significantly higher than those of controls (p < 0.001). The lead level of the battery workers was also significantly higher than that of muffler repair workers (p < 0.001). Although, statisticly significant, higher blood lead levels are not related to toxicity for battery and muffler repair workers. Total protein, globulin, cholesterol, LDH, and ALP levels were within normal levels, however, they were slightly higher than the control levels. Increased LDH among the workers seems to be related rather to other causes than to the liver injury.

[Some hematologic values of Peking ducks]. / Einige hämatologische Werte bei Peking-Enten.

This work has been done to investigate physiological values of some hematological parameters of peking ducks. For this purpose 20 healthy peking ducks have been studied. Total red (R.B.C.) and white (W.B.C.) blood cell counts by routine methods in Thoma hemocytometers after diluting with Natt-Herrick solution, packed cell volume (P.C.V. = Htc) by the microhematocrit centrifuge method, hemoglobin (Hb) by the cyanmethaemoglobin method were carried out. Blood films were stained by Pappenheim's method and the percentage of neutrophils, lymphocytes, eosinophils, basophils, and monocytes was estimated on a differential count of 200 cells. The mean values have been found as follows: R.B.C. = 3,835 x 10(6)/mm3, W.B.C. = 15.950/mm3, Hb = 12 g%, P.C.V. = 36,15%, neutrophils = 62,10%, lymphocytes = 30,95%, basophils = 5,8%, eosinophils = 0,6% [corrected], monocytes = 0,6%.

Effect of nicotine exposure during gestation on neonatal rat crystalline lenses.

PURPOSE: To assess histologically the influence of maternal nicotine exposure during gestation in vivo on crystalline lenses in neonatal rats using different dosages of the test compound simulating the range of low, moderate, and heavy smokers in humans. METHODS: Experimentally naive, adult female Wistar-albino rats (200-250 g) were mated with adult male rats over 2 days for copulation in the proportion of two females for every male animal. After confirming pregnancy with vaginal smear method, 40 gravid rats (dams) were then randomly assigned into four equal groups (three experimental and one control; n=10 in each). Groups 1, 2, and 3 experimental dams were treated with intraperitoneal (i.p.) (-)-nicotine tartrate at doses of 0.5, 1, and 2 mg/kg body weight/day, respectively, during pregnancy from gestational days 9 through 21. Group 4 control dams were given i.p. saline solution daily for the same period. After normal delivery, the eyes were removed at postnatal day 1 or day 30 for macroscopic and histopathologic investigation of the lenses. RESULTS: Control and group 1 litters had normal anterior lens capsules with a single layer of anterior cuboidal epithelial cells, regularly orientated cortical and nuclear lens fibres, and a clear posterior lens capsule with no lining epithelial cells behind the equator. On the other hand, some lenses in groups 2 and 3 litters had mature or immature cataract macroscopically at postnatal 30th day. Histopathologic findings suggesting cataractogenesis included cortical lens fibre cell swelling and liquefaction, prominent epithelial cells lining the posterior lens capsule behind the equator, and the retention of lens nuclei into the deeper and central area. Moreover, some lenses were immature developmentally, indicating arrested lenticular embryogenesis at vesicle stage. CONCLUSIONS: Nicotine exposure during pregnancy has teratogenic and cataractogenic effects on developing crystalline lenses in neonatal rats both macroscopically and histopathologically. If appropriate dose of nicotine can be identified, nicotine-induced cataract formation may possibly be used as a new experimental cataract model in animal studies. Therefore, future studies are needed in this respect. Eye (2004) 18, 67-73. doi:10.1038/sj.eye.6700511

Blood lead levels of the battery and exhaust workers and their pulmonary function tests.

In an attempt to understand the impact of inhaled lead on the pulmonary functions, we assessed the blood lead levels and pulmonary functions of the battery and exhaust workers who are potential candidates for lead inhalation. The hospital staff served as control group. The measurements of lead levels were performed using atomic absorption spectrophotometry. Pulmonary function tests (PFTs) were performed using a portable spirometer. The blood lead levels of the battery workers, exhaust workers and controls were found to be 36.83, 26.94 and 14.81 microg/dl, respectively. The values of the workers were significantly higher than the controls (p < 0.001). The lead levels of the battery workers were also significantly higher than the exhaust workers (p < 0.001). PFT results (maximum voluntary ventilation, forced expiration flow and first forced expiration volume values of the workers) were significantly worse than the controls, and their pulmonary function test results were consistent with restrictive problems in the airways.

Long-term pulmonary histopathologic changes in rats following acute experimental exposure to chlorine gas.

In this study, we aimed to investigate the long-term histopathologic changes in the lungs of rats exposed to a high concentration of chlorine gas. Twenty-four Sprague-Dawley rats were divided into three groups: the control group (group I) (n = 8), early-examined group (group II) (n = 8), and late-examined group (group III) (n = 8). In group II the lungs of rats were taken out just after the exposure, whereas in group III the lungs were taken out 45 days after the exposure. Eosinophilic liquid accumulation in alveoli and bronchi, diffuse intraalveolar edema, vascular congestion, severe perivascular edema, and free bleeding in intraalveolar and interstitial area were observed in the lungs of rats in group II. Interstitial fibrosis and thickening of the alveolar septa were observed in group III. These findings suggest that the people using these cleaning agents are at risk of harming themselves, and the victims of chlorine gas injury should be reexamined at a later period since they may have pulmonary damage even after 45 days of exposure.