Gibberellic acid acts as an agonist of steroidogenesis in male rats

Testicular steroidogenesis has significant implication in male reproductive function. Although the effects of various signalling molecules on testicular functions have been studied earlier, the influence of the plant hormone gibberellic acid (GA₃) on steroidogenesis has not been investigated. Acute (4 h) and subacute (15 days) studies using this compound through oral administration (150 μg day^?1) to groups of normal and diabetic Wistar male rats were therefore carried out. Results indicate that (i) enhanced activity of steroidogenic markers 3β‐hydroxysteroid dehydrogenase (3β‐HSD), 17β‐hydroxysteroid dehydrogenase (17β‐HSD), elevated tissue testosterone (T) content, increased steroidogenic acute regulatory protein (StAR) and androgen binding protein (ABP) levels with reduced lipid peroxidation and improved antioxidant defence in this treatment group of normal and diabetic rat testis, and (ii) elevated lipid peroxidation and diminished antioxidant defence, with insignificant change in 3β‐HSD and 17β‐HSD activity and testosterone level in acute treatment group of normal and diabetic rats testis, were noted. The observed increase in the activity of testicular 3β‐HSD and 17β‐HSD along with elevated testosterone content established GA₃ as an inducer of steroidogenesis in rat.     

The reproductive system of male rats exposed to very low doses of ionizing radiation, 1: Hormonal profile of animals exposed after sexual maturity

Adult male rats were treated with a single, whole body exposure to a dose of 0.001, 0.01 or 0.1 Gy (1 Gy = 100 rad). The animals were sacrificed 1, 7, 30, 100 or 180 days following exposure. Serum testosterone, serum and hypophyseal LH, FSH and prolactin as well as hypothalamic LHRH were measured. In the 0.1 Gy irradiated rats, serum LH and FSH were 100% higher and serum prolactin was 30% lower as compared to controls, 30 days after irradiation. The concentrations of these hormones remained significantly different from control values even after 180 days after exposure. On the other hand, the hypophyseal content of LH, FSH and prolactin decreased in the 0.1 Gy treated rats, 100 days after irradiation. In the group of the 0.01 Gy irradiated rats, serum FSH increased by 70% and hypophyseal FSH decreased. No changes were observed in serum testosterone and hypothalamic LHRH in any of the irradiated groups and no changes were observed in the group exposed to 0.001 Gy. It may be concluded that a long term damage to the reproductive system of the male rat was induced by a single, whole body exposure to 0.1 Gy of gamma radiation.     

Modification in oxidative processes in muscle tissues exposed to laser- and light-emitting diode radiation

Exposure of living tissues to high-intensity red or near-infrared light can produce the oxidative stress effects both in the target zone and adjacent ones. The protein oxidative modification (POM) products can be used as reliable and early markers of oxidative stress. The contents of modified proteins in the investigated specimens can be evaluated by the 2,4-dinitrophenylhydrazine assay (the DNPH assay). Low-intensity red light is able to decrease the activity of oxidative processes and the DNPH assay data about the POM products in the biological tissues could show both an oxidative stress level and an efficiency of physical agent protection against the oxidative processes. Two control groups of white rats were irradiated by laser light, the first control group by red light and the second one by near-infrared radiation (NIR).Two experimental groups were consequently treated with laser and red low-level light-emitting diode radiation (LED). One of them was exposed to red laser light + LED and the other to NIR + LED. The fifth group was intact. Each group included ten animals. The effect of laser light was studied by methods of protein oxidative modifications. We measured levels of both induced and spontaneous POM products by the DNPH assay. The dramatic increase in levels of POM products in the control group samples when compared with the intact group data as well as the sharp decrease in the POM products in the experimental groups treated with LED low-level light were statistically significant (p ≤ 0.05). Exposure of skeletal muscles to high-intensity red and near-infrared laser light causes oxidative stress that continues not less than 3 days. The method of measurement of POM product contents by the DNPH assay is a reliable test of an oxidative process rate. Red low-intensity LED radiation can provide rehabilitation of skeletal muscle tissues treated with high-intensity laser light.     

Dexmedetomidine protects against myocardial ischaemia/reperfusion-induced renal damage in rats

Background

Myocardial ischaemia/reperfusion (MI/R) may induce renal damage. Our aim was to investigate the effects of dexmedetomidine (DEX) administration at two different timings either before or after ischaemia on renal damage induced by MI/R.

Preclinical efficacy of Dexmedetomidine on spinal cord injury provoked oxidative renal damage

Abstract

Purpose: Oxidative renal injury is the mainstay in patients with spinal cord injury (SCI) and it may eventuate to chronic renal failure. In our study, we investigated the potential of α2-adrenoreceptor agonist Dexmedetomidine (Dex) in ameliorating SCI provoked oxidative renal assault. Methods: Complete SCI was generated by surgical transaction of the cord at the T10–12 level. Dex administration (50?mcg/kg, b.wt, intraperitoneally) was initiated 12?h after the surgery for 10 days. Then, blood was collected and kidneys were removed to evaluate the efficacy of Dex on post-SCI renal complications. Results: Dex treatment significantly attenuated elevated serum creatinine and blood urea nitrogen in SCI rats to normalcy. Further in SCI rats elevated level of MDA, protein carbonyl and myeloperoxidase (MPO) were observed and Dex treatment significantly attenuated these toxic manifestations to normalcy. Besides in SCI rats, the antioxidants (SOD, CAT, Gpx and GST and GSH) levels were significantly diminished and Dex treated rats significantly restored the antioxidants level in renal tissue to normalcy. Notably, in our study the protein expression of inflammatory cytokines (TNF-α and IL-6) and cleaved caspase-3 were upregulated in renal tissue of SCI rats. Fascinatingly, Dex treatment downregulated the protein expression of TNF-α, IL-6 and cleaved caspase-3 by anti-inflammatory, antiapoptotic mechanism. Furthermore, SCI rats displayed upregulated protein expression of kidney of SCI rats. Dex treatment diminished the renal apoptosis by downregulating the cleaved caspase-3 expression. Conclusion: Taken together, these results accentuate that Dex may be a beneficial clinical agent to combat post-SCI renal complications.     

Osteogenesis in exposure to ionizing radiation in vitro

Irradiation is a well established therapeutical concept to prevent heterotopic ossification after joint replacement. The influence of irradiation on proliferation of mature osteoblasts and their potential osteoprogenitors, matrix formation and mineralization are not well known in this setting. We therefore studied the effect of different doses of ionizing irradiation on the several steps of osteogenesis in vitro, using cells isolated from the juvenile rat. A colony forming test, the MTT-viability assay, a cell count, measurement of the cellular protein content and alkaline phosphatase activity, as well as determination of in vitro mineralisation have been applied to calvarian osteoblasts, fibroblasts and stromal bone marrow cells. Irradiation results in a dose-dependent suppression of clonogenic activity in all mitotically active cells, but metabolic activity and matrix synthesis were not impaired. In dense cultures alkaline phosphatase expression and in vitro mineralisation were not significantly affected by irradiation. Our experimental in vitro data suggest that irradiation inhibits the initial phase of in vivo osteogenesis due to the cytostatic effect. Postoperative irradiation after THR must therefore take place as early as possible. The homoeostasis of normal, orthotopic bone does not seem to be severely affected by local low-dose irradiation.     

Cornea epithelial damage thresholds in rabbits exposed to Tm:YAG laser radiation at 2.02 microns.

We have determined exposure conditions for minimal damage to the corneal epithelium in rabbit using a continuous wave Tm: YAG laser operating in the TEM00 mode at incident powers between 80 and 450 mW. The 1/e beam diameter was 0.94 mm and exposure durations for threshold damage ranged from 4.3 to 0.08 sec. Calculated temperature increases on the beam axis 10 microns beneath the surface at the measured thresholds were essentially constant and averaged 44 degrees C. This is basically the same temperature increase found for threshold CO2 laser damage and suggests that the critical temperature damage model, which correlates CO2 laser damage, can predict damage thresholds for mid-infrared laser radiation. We also showed that reliable thresholds can be determined in freshly enucleated eyes, thus opening up the possibility of using available laser sources in laboratories not equipped and approved for animal experiments to determine damage thresholds.     

Staff exposure to ionizing radiation in a major trauma centre

BACKGROUND: The purpose of the present paper was to determine the safety of staff members with regard to ionizing radiation in a major trauma centre in a 19-month period. METHODS AND RESULTS: A group of five doctors, five nurses and a trauma orderly wore personal radiation monitors under lead aprons while at work. The highest individual cumulative result after 586 days was 0.18 mSv for a nurse. If the exposure rate to ionizing radiation was constant, this would be equivalent to 0.114 mSv per year. Therefore the results are well below the recommended occupational dose limit of 20 mSv per year. CONCLUSION: Wearing of lead aprons during trauma resuscitation appears to be safe and provides adequate protection.     

Dexmedetomidine as an Anesthetic Adjunct in Coronary Artery Bypass Grafting

Background: Alpha2 -Adrenergic agonists decrease sympathetic tone with ensuing attenuation of neuroendocrine and hemodynamic responses to anesthesia and surgery. The effects of dexmedetomidine, a highly specific alpha2 -adrenergic agonist, on these responses have not been reported in patients undergoing coronary artery bypass grafting.

Methods: Eighty patients scheduled for elective coronary artery bypass grafting received, in a double-blind manner, either a saline placebo or a dexmedetomidine infusion, initially 50 ng [center dot] kg-1 [center dot] min-1 for 30 min before induction of anesthesia with fentanyl, and then 7 ng [center dot] kg-1 [center dot] min-1 until the end of surgery. Filling pressures, blood pressure, and heart rate were controlled by intravenous fluid and by supplemental anesthetics and vasoactive drugs.

Results: Compared with placebo, dexmedetomidine decreased plasma norepinephrine concentrations by 90%, attenuated the increase of blood pressure during anesthesia (3 vs. 24 mmHg) and surgery (2 vs. 14 mmHg), but increased slightly the need for intravenous fluid challenge (29 vs. 20 patients) and induced more hypotension during cardiopulmonary bypass (9 vs. 0 patients). Dexmedetomidine decreased the incidence of intraoperative (2 vs. 13 patients) and postoperative (5 vs. 16 patients) tachycardia. Dexmedetomidine also decreased the need for additional doses of fentanyl (3.1 vs. 5.4), the increments of enflurane (4.4 vs. 5.6), the need for beta blockers (3 vs. 11 patients), and the incidence of fentanyl-induced muscle rigidity (15 vs. 33 patients) and postoperative shivering (13 vs. 23 patients).     

Carob attenuates nicotine-induced oxidative stress and intratesticular damage in male rats

In this study, we aimed to evaluate the effect of carob extract against intratesticular histological, apoptotic, biochemical and spermatogenic changes in rats exposed to nicotine. Twenty-eight rats were divided into four groups and were administered saline, nicotine, carob, or nicotine + carob once a day for 35 days. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX), GSH, total anti-oxidative status (TAS), total oxidative status (TOS), oxidative stress index (OSI), IL-6, TNF-α and seminal parameters were evaluated. Johnsen's testicular histopathological examination, factor VIII protein (angiogenesis marker) and the number of apoptotic cells were determined in the testicular tissues. The spermatogenic and histopathological examination revealed that nicotine + carob group had significant positive changes in seminal parameters, Johnsen score, apoptotic cell count and factor VIII protein compared to nicotine group. Biochemical test results indicated that the nicotine + carob group had significantly lower TAS levels compared to the control group; however, those levels were higher than those of the nicotine group. Nicotine caused a significant increase in IL-6 and TNF-α levels compared to the control group, but carob seems to significantly counteract that increase. In conclusion, carob extract had positive effects on spermatogenesis and reduced testicular parenchymal damage, apoptosis and angiogenesis.     

Impact of naringenin on oxytetracycline-mediated oxidative damage in kidney of rats

The aim of this study was to investigate the effect of naringenin on oxytetracycline-induced nephrotoxicity in rats. Oxytetracycline (200 mg/kg body weight, ip) was administered in 0.5 ml of sterile physiological saline for 15 days, resulting in a significant increase in serum urea and creatinine and reduction in creatinine clearance. A significant increase in lipid peroxidation markers (TBARS and lipid hydroperoxide) and decrease in antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase) and low molecular weight antioxidants (vitamin C, vitamin E, and reduced glutathione) levels were also observed in oxytetracycline-treated rats. The oral administration of naringenin (50 mg/kg body weight) attenuated the oxytetracycline-induced nephrotoxicity by significantly decreased levels of serum urea and creatinine with the significant normalization of creatinine clearance. Upon the administration of naringenin, the depleted renal antioxidant defense system (enzymatic and non-enzymatic antioxidants) was significantly increased in rats treated with oxytetracycline. These biochemical observations were supplemented by histopathological examination of kidney section. The present results suggest that the supplementation of naringenin might be helpful to alleviate the oxytetracycline-induced oxidative injury in kidney.     

The effects of N-acetylcysteine on methotrexate-induced oxidative renal damage in rats.

Sir, Methotrexate (MTX), a folic acid antagonist, is widely usedas a cytotoxic chemotherapeutic agent for several malignanciesand various inflammatory diseases. However, the efficacy ofthis agent often is limited by severe side effects and toxicconditions. MTX     

Quercetin ameliorates methotrexate-induced renal damage,apoptosis and oxidative stress in rats

Abstract

Background: In the present study, the protective and therapeutic effects of quercetin (QE) on renal injury induced by methotrexate (MTX) have been examined. Materials and methods: A total of 24 male rats were divided into the following three groups: control group, MTX group, and MTX?+?QE group. Rats in MTX group received 20?mg/kg of single dose of MTX, while those in MTX?+?QE group received 20?mg/kg of single dose MTX, in addition to 15?mg/kg of QE administered 30?min prior to MTX and in the following 5-day period as a single daily dose. At the end of the experimental period, renal tissues were removed for histopathological and biochemical assessments. Results: Light microscopic examination showed a disruption of the renal structure in rats in MTX group in the form of tubular degeneration and dilation, with shedding of the tubular epithelial cells into the lumen. QE treatment was associated with less marked degenerative changes, with a similar histological appearance to that of controls. Furthermore, QE treatment resulted in decreased the number of apoptotic cells. Biochemical assessments showed significantly higher malondialdehyde (MDA) levels in MTX group as compared to control and MTX?+?QE groups. superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) levels showed a significant decrease in MTX group as compared to controls. However, QE significantly suppressed MDA level, compensated deficits in the anti-oxidant defenses [reduced SOD, GSH-Px, and CAT levels] in kidney tissue resulted from MTX administration. Conclusions: In conclusion, renal toxic effects of MTX may be alleviated by QE.