Changes in Angiotensin Converting Enzyme in Testes and Epididymes of Rat Due to Serotonin Administration

Effect of exogenous serotonin and blockade of its endogenous production on Angiotensin Converting Enzyme (ACE) in testes and epididymis was studied. Serotonin (30 mg/kg) and p-chlorophenylalanine (100 mg/kg) were injected for 4 and 3 days respectively. Serotonin reduced the weights of testes, seminal vesicle and ventral prostate whereas epididymal weight increased due to fluid accumulation. ACE was significantly reduced in tissue and fluid fractions of testes and epididymis of serotonin treated rats. pCPA had no effect on ACE levels. Serotonin seems to have direct effect on epididymis also.     

Endocrine Effects of Early Non-Union of Testis and Epididymis and of Cryptorchidism in the Rat/Endokrine Effekte bei jungen Ratten nach experimenteller Trennung von Hoden und Nebenhoden wie auch nach experimentellem Kryptorchismus

The aim of this study was to explore possible endocrine effects of early non-union of testis and epididymis. In 16 days old Sprague-Dawley rats the testis and epididymis were separated to the level of the inferior epididymis artery (non-union operation). Animals were killed at intervals from 30-58 days, and the plasma concentrations of total testosterone, total estrogens, LH, FSH and PRL were measured. The testes were studied by light microscopy. Groups of rats made cryptorchid and sham-operated rats were used as controls. Although their testes were scrotal, the non-union operated animals had testosterone and estrogen concentrations similar of cryptorchid animals, and significantly (p less than 0.05) lower than sham-operated animals. The LH- and FSH-concentrations were significantly (p less than 0.05) elevated suggesting a primary lesion in both Leydig- and Sertoli-cells. Towards puberty FSH increased in the non-union operated animals, while FSH values declined in the cryptorchid and sham-operated animals. These FSH-patterns probably reflect the existence of different pathogenic mechanisms in the non-union operated rats and the rats with cryptorchid testes.     

Angiotensin Converting Enzyme in the Testis and Epididymis of Mammals

Summary: Angiotensin converting enzyme (ACE) activity has been reported in testis and epididymis of seven different animal species. Among all the species, the mouse testis and epididymis showed the highest converting enzyme activity followed by rat testis and epididymis. The lowest activity was detected in buffalo testis and rabbit epididymis. Most of the testicular enzyme was found concentrated in the 107,00 xg sediment while the epididymal enzyme was equally distributed between sediment and supernatant. ACE levels of different regions of the rat testis and epididymis was analyzed. The gradient of ACE was found increasing from caput to cauda. A major fraction of testicular and epididymal ACE activity was found in their respective fluid. ACE appeared only in mature rats, rabbits and mice testis and epididymis. Sexually stimulated rabbits showed significant ACE increase in the testis. In vitro characterization studies were conducted. Zusammenfassung: Angiotensin-Converting-Enzym in den Hoden und Nebenhoden von Säugetieren Es wird berichtet über die Aktivität des Angiotensin-Converting-Enzyms (ACE) in den Hoden und Nebenhoden sieben verschiedener Tierarten. Von alien Arten zeigten die Hoden und Nebenhoden der Maus die höchste Enzymaktivität, gefolgt von den Hoden und Nebenhoden der Ratte. Die niedrigste Aktivität wurde in Büffelhoden und Kaninchennebenhoden gefunden. Der größte Teil des Hodenenzyms was in dem UI-trazentrifugensediment (107.000 × g) konzentriert, wohingegen das Nebenhodenenzym gleichmäßig auf das Sediment und den Überstand verteilt waren. Es wurden die ACE-Konzentrationen verschiedener Anteile des Rattenhodens und -nebenhodens bestimmt. Die ACE-Konzentration nahm dabei vom Kopf zum Schwanz hin zu. Der Hauptanteil der Hoden- und Nebenhoden-ACE-Aktivität wurde in den jeweiligen Flüssigkeitsanteilen gefunden. Das ACE tritt nur in geschlechtsreifen Ratten-, Kaninchen- und Mäusehoden und -nebenhoden auf. Sexuell stimulierte Kaninchen wiesen einen signifikanten ACE-Anstieg in den Hoden auf. Die Untersuchungen zur in-vitro-Bestimmung wurden aufgezeigt.     

Renal angiotensin converting enzyme (ACE) expression in diabetic rats: the effect of ACE inhibitors]

Renal excreted angiotensin converting enzyme (ACE) inhibitor captopril, and renal.hepatic bile excreted ACE inhibitor temocapril, were compared by monitoring serum ACE and renal ACE expression (protein and mRNA) in streptozotocin-induced diabetic rats. Serum ACE levels did not change in untreated diabetic rats or in those treated with temocapril, compared with normal control rats. However, serum ACE levels significantly increased in diabetic rats treated with captopril after 3 months (153.8 +/- 23.0 vs. 43.5 +/- 5.5 IU/l/37 degrees C, p < 0.01) and 6 months (113.6 +/- 9.3 vs. 36.9 +/- 2.9 IU/l/37 degrees C, p < 0.01) compared with normal control rats. Compared with normal control rats (3.6 +/- 0.4), proximal tubular ACE protein expression significantly (p < 0.01) decreased in untreated diabetic rats (1.6 +/- 1.1), but significantly (p < 0.01) increased in diabetic rats treated with captopril (3.7 +/- 0.3) and temocapril (3.5 +/- 0.4). Renal ACE mRNA levels decreased in untreated diabetic rats (125.5 +/- 20.3 vs. 313.3 +/- 53.4, p < 0.01) compared with normal control rats for 6 months. Renal ACE mRNA levels tended to increase in diabetic rats treated with captopril (184.4 +/- 51.2 vs. 125.5 +/- 20.3) and temocapril (165.4 +/- 43.2 vs. 125.5 +/- 20.3) compared with untreated diabetic rats for 6 months. In conclusion, diabetic rats had lower proximal tubular ACE protein expression and lower renal ACE mRNA levels compared with normal control rats. Furthermore, both ACE inhibitors increased renal ACE protein and mRNA expression, but differed in their effect on serum ACE levels.     

Antispermatogenic/antiandrogenic properties of solasodine (C27H43O2N) obtained from solanum xanthocarpum berries on the male genital tract of dog (Canis-familiaris). A Histophysiological approach

Chronic administration of solasodine (20 mg/kg alt. day for 30 days) caused testicular lesions resulting in a severe impairment of spermatogenic elements. The epididymides were devoid of spermatozoa. Total protein, sialic acid and glycogen contents of the testis and epididymis were reduced significantly whereas the testicular cholesterol was elevated. Acid Phosphatase enzyme activity of the testes was low after solasodine treatment. Serum enzymes (SGPT, alkaline phosphatase) serum protein, triglycerides, non esterified fatty acid levels were in normal range when compared with their own controls. Cholesterol and phospholipid levels were elevated after solasodine treatment to intact dogs. Reduced androgen production was reflected in low levels of sialic acid in the testes and epididymides and reduced Leydig cell nuclei. Castration alone brought about reduction in size of the epididymis. Castration followed by solasodine treatment caused epididymal degeneration. Simultaneous administration of TP to solasodine treated castrated dogs failed to stimulate the epididymal growth. Antispermatogenic/antiandrogenic activity of the compound solasodine is discussed. Solasodine administration in dogs definitely rendered the male infertile as evidenced by the absence of sperms in the cauda epididymis and ductus deferens.     

Production of Angiotensin-Converting Enzyme in Rat Epididymis

Unilateral ductuli efferentia testis of immature rat were severed in order to interrupt the continuity between testis and epididymis and angiotensin-converting enzyme (ACE) activities were measured 5 weeks after the operation. The epididymal ACE on the operated side increased to nearly the same level as that on the contralateral side, but the testicular ACE activity on the operated side was markedly lower than that on the contralateral side. On immunofluorescent study using antiserum against purified rat lung ACE, ACE could be found in the tubular epithelial cells of the operated epididymis. These results suggest that epididymis itself synthesize ACE without connection to testis.     

Angiotensin converting enzyme in human seminal plasma is synthesized by the testis, epididymis and prostate

The activity of angiotensin converting enzyme (ACE) was assessed in human body fluids (serum, seminal plasma, prostatic secretions), in tissue extracts of the testis, epididymis, prostate and skeletal muscle, in split ejaculates and in seminal plasma obtained from patients before and after vasectomy. To ensure the specificity of the results the dependence of ACE activity on specific inhibitors was evaluated. Enzyme activity found in tissues of the male genital tract was considerably higher than that in serum and other tissues. ACE in human seminal plasma is synthesized by the testis, epididymis and prostate in different amounts.     

Oxidative and antioxidative status in the testes of rats with acute epididymitis

INTRODUCTION: Epididymitis is an inflammation or infection of the epididymis, a convoluted duct that lies on the posterior surface of the testicle. Oxidative stress due to excessive production of reactive oxygen species in epididymitis, impaired antioxidant defense mechanisms, or both, precipitates a range of pathologies that are currently believed to negatively affect the male reproductive function. How oxidative stress affects the testes is still unknown. We aimed to investigate the oxidative and antioxidative status of testes of rats with unilateral acute Escherichia coli epididymitis. METHODS: The study included 36 male Wistar albino rats which were divided into three groups. In the epididymitis group (n = 12), an E. coli suspension was injected into the right ductus deferens of rats, and the same amount of saline was injected in the saline groups (n = 12). No surgery was performed in the control group (n = 12) for baseline values. Rats were sacrificed after 24 h and the epididymis and testes removed. The infection was confirmed by histopathologic evaluation and microbiological tests. The oxidative status of testes was evaluated by measuring myeloperoxidase (MPO) activity, and antioxidative status was evaluated by measuring total antioxidant response (TAR) and total antioxidant capacity levels (TAC). RESULTS: MPO activity in both the ipsilateral and contralateral testes of the epididymitis group was significantly higher than those of the saline and control groups (p < 0.05). The TAR and TAC levels in both testes were also significantly elevated in the epididymitis group versus the two other groups (p < 0.05). CONCLUSIONS: Acute epididymitis causes an increase of oxidative stress in the ipsilateral and contralateral testes, but this condition is strived for to tolerate the increase of endogenous antioxidants.     

生精冲剂对精索静脉曲张大鼠睾丸生精功能的作用

目的:探讨生精冲剂对精索静脉曲张睾丸损伤的作用.方法:观察生精冲剂对实验性精索静脉曲张大鼠睾丸组织结构、超微结构的影响.测定各组实验大鼠睾丸SOD、CAT、ACE活性和LPO、NO含量.结果:治疗组鼠睾丸组织结构与超微结构的损害程度明显低于模型组;SOD、CAT、ACE活性测定值明显高于模型组,LPO、NO含量明显低于模型组(P<0.05).结论:生精冲剂对精索静脉曲张造成的睾丸损害有保护作用,其提高精液质量和生育率的机制可能与抗脂质过氧化和增强抗氧化酶活性有关.     

Angiotensin-converting enzyme inhibition attenuates hypercholesterolemia and glomerular injury in hyperlipidemic Imai rats.

Hyperlipidemic Imai rats spontaneously develop hypercholesterolemia, proteinuria and glomerulosclerosis. We investigated the effect of enalapril, an angiotensin-converting enzyme (ACE) inhibitor, on spontaneous hypercholesterolemia and the progressive renal injury in this rat strain. Male Imai rats (n = 7) were treated with enalapril at a dose of 50 mg/l in drinking water starting at 6 weeks of age. Body weight, blood pressure, urinary protein excretion and serum constituents were checked and compared with untreated controls (n = 5) up to 38 weeks of age. Enalapril treatment significantly reduced hypercholesterolemia (247 +/- 41 vs. 102 +/- 13 mg/dl, p < 0.01, at 38 weeks) and proteinuria (766 +/- 290 vs. 206 +/- 119 mg/kg/day, p < 0.01, at 38 weeks). The glomerulosclerosis index (SI) was significantly higher in untreated control rats than in the enalapril-treated group (227 +/- 57 vs. 27 +/- 9, p < 0.01). Although we could not clarify whether hypercholesterolemia is a primary event or secondary to the nephrotic syndrome, these results indicate that the ACE inhibitor has the property to protect remnant glomeruli from glomerulosclerosis in male Imai rats as well as in other animal models in which focal and segmental glomerulosclerosis is believed to represent a common pathologic pattern. This rat strain represents a unique model of a spontaneous proteinuria which can provide an important information on the pathogenesis of human focal and segmental glomerulosclerosis.     

可卡因诱导不同年龄段大鼠生精细胞凋亡及Caspase-3活性研究

目的　探讨可卡因对不同年龄段大鼠生精细胞凋亡的影响。方法　应用 3周、6周和 12周龄S D雄性大鼠皮下注射可卡因 2 8d制造吸毒动物模型。采用放射免疫法测定血清LH、FSH、PRL、T、E2 浓度 ,DNA片段和流式细胞术分析生殖细胞凋亡状况 ,Caspase 3活性。 结果　可卡因诱导 2周后 ,3周龄大鼠睾丸重量减轻 (P <0 .0 5 ) ,体重及其他生殖器官重量无明显影响 ;6周龄大鼠体重、睾丸、附睾和阴茎重量减轻 (P <0 .0 1) ;12周龄大鼠体重和生殖器官重量则均无明显影响 (P >0 .0 5 )。 3周龄实验组大鼠T降低 ,E2 升高 ,差异有显著意义 (P <0 .0 5 ) ,LH、FSH和PRL无明显差异 ;6周龄实验组大鼠LH和T明显降低 ,FSH明显升高 (P <0 .0 5 ) ,而PRL和E2变化 ;12周龄实验组大鼠PRL有明显降低 (P <0 .0 1) ,余无显著差异。 3个年龄段实验组大鼠均出现细胞凋亡梯带 ,其中 6周龄组最为典型。 3周龄和 6周龄实验大鼠生精细胞凋亡峰值明显增高。S期细胞数明显下降 ,其中尤以 6周龄大鼠显著。 3周龄、6周龄和 12周龄实验组大鼠睾丸生精细胞Caspase 3活性均较对照组明显增高 ,其中6周龄实验组Caspase 3活性增高更为明显 (P <0 .0 1)。 结论　可卡因诱导 2 8天可致大鼠生殖器官发育和生殖内分泌功能损害 ,造成生精细胞凋亡增加 ,增     

Lung angiotensin converting enzyme activity in rats with pulmonary hypertension.

We have studied serum and lung tissue angiotensin converting enzyme (ACE) activity in female Wistar rats with pulmonary hypertension induced by two different methods. Chronic pulmonary hypertension was produced in one group of 10 rats (CH) by confinement in a hypobaric chamber (380 mmHg) for three weeks, and in another group fo 10 rats (M) by a single subcutaneous injection of monocrotaline (60 mg/kg body weight). In these two groups of tests rats and in 20 untreated controls (C), we evaluated right ventricular mean systolic blood pressure (Prvs mmHg), right ventricular hypertrophy, and serum ACE (n mol/ml/min). In lung tissue homogenate, we measured the specific activity of ACE (n mol/mg protein/min), alkaline phosphatase (AP) (IU/mg protein) and lactic dehydrogenase (LDH) (IU/mg protein). The Prvs in groups, C, CH, and M was 25 +/- 7 SD, 41 +/- 7, and 51 +/- 5, respectively. The ratio of right ot left ventricular weight (RV/(LV + S)%) in groups, C, CH, and M was 29 +/- 4, 52 +/- 5, and 56 +/- 7, respectively. The lung tissue ACE in groups C, CH, and M was 85 +/- 11, 65 +/- 20, and 22 +/- 5, respectively. In groups CH, and M the Prvs and RV/(LV + S)% were significantly elevated above control values while lung ACE was significant decreased (p less than 0.05). There was a significant inverse relationship between lung ACE on one hand, and Prvs (r = - 0.73) and RV/(LV + S)% (r = - 0.71) on the other hand. Serum ACE and lung AP were unchanged. In group M there was a slight but significant reduction in lung LDH. Chronic pulmonary hypertension, irrespective of its method of production, is associated with decreased lung ACE. The reduction in lung ACE is inversely proportional to the severity of pulmonary hypertension and right ventricular hypertrophy.     

Fat redistribution and adipocyte transformation in uninephrectomized rats

Dyslipidemia complicates renal function leading to disturbances of major homeostatic organs in the body. Here we examined the effect of chronic renal dysfunction induced by uninephrectomy on fat redistribution and lipid peroxidation in rats treated with an angiotensin-converting enzyme (ACE) inhibitor (lisinopril) for up to 10 months. Uninephrectomized rats developed fat redistribution and hypercholesterolemia typical of chronic renal failure when compared with sham-operated rats or lisinopril-treated uninephrectomized rats. The weight of the peri-renal fat was significantly less in the untreated compared to the lisinopril-treated uninephrectomized rats or those rats with a sham operation. We also found that there was a shift of heat-protecting unilocular adipocytes to heat-producing multilocular fat cells in the untreated uninephrectomized rats. Similarly in these rats we found a shift of subcutaneous and visceral fat to ectopic fat with excessive lipid accumulation and lipofuscin pigmentation. Lisinopril treatment prevented fat redistribution or transformation and lipid peroxidation. This study shows that ACE inhibition may prevent the fat anomalies associated with chronic renal dysfunction.     

Time-specific effects of mono-n-butyl phthalate on the transabdominal descent of the testis in rat fetuses

OBJECTIVE: To determine the time-specific effects of mono-n-butyl phthalate (MBP) on the transabdominal migration of the testis in fetal rats. Materials and methods Three groups of pregnant rats were administered MBP by stomach-tube feeding when the fetus was at 7-10 days of gestation in group 1, 11-14 days in group 2, and 15-18 days in group 3; controls (group 4) were given vehicle only from 7-18 days. At 20 days of gestation the fetuses were obtained by Caesarean section, and the position of the testes, the development of the gubernaculum, cranial suspensory ligament and the epididymis were examined. RESULTS: The timed intervals of MBP administration showed that the maximum inhibition of transabdominal testicular descent was at 15-18 days of gestation. There was an elongated gubernaculum and hypertrophic cranial suspensory ligament in the MBP-treated rat fetuses. Furthermore, the epididymis showed a few small ducti deferentia, although there were no remarkable changes in either the Sertoli and Leydig cells in these testes. The mean (SEM) content of testicular testosterone was significantly less (P < 0.001) in the MBP-treated rats, at 50.9 (3.8) pg/testis, than in the controls, at 676 (33.3) pg/testis. CONCLUSIONS: These findings indicate that a brief exposure to MBP during fetal development can inhibit the transabdominal migration of the testis and reduce testosterone content in rats, although the relationship between migration and the testicular testosterone content remains unknown.     

Effects of ACE inhibition and bradykinin antagonism on cardiovascular changes in uremic rats

BACKGROUND: Cardiovascular death continues to be a major problem in renal failure. Structural abnormalities of the heart and the vasculature contribute to the increased cardiovascular risk. They are ameliorated by angiotensin-converting enzyme (ACE) inhibitors, but because of the nonspecifity of ACE inhibition, it is uncertain whether the beneficial effect is mediated by interfering with angiotensin II (Ang II) or by modulating other effector systems, for example, bradykinin. METHODS: To assess a potential role of bradykinin, subtotally nephrectomized Sprague-Dawley rats (SNX) received either the ACE inhibitor Ramipril (Rami, 0.2 mg/kg body weight p.o.), the specific B2 bradykinin receptor antagonist Hoe140 (0.2 mg/kg body weight, s.c.), or a combination of both, and were compared to sham-operated controls. To separately assess the effect of Ramipril on development and reversal of structural abnormalities, animals were either treated from the third day after SNX or from the fourth week after SNX onward (0.01 mg/kg body weight, p.o.). RESULTS: Heart and aorta were evaluated by morphometric and stereologic techniques. The weight of the perfused left ventricle, as an index of cardiac hypertrophy, was significantly higher in untreated SNX. While it was significantly lower in animals with early and late Ramipril treatment, the beneficial effect was completely antagonized by Hoe140. The wall-to-lumen ratio of intramyocardial arterioles was significantly higher in untreated SNX compared with controls, but failed to be modified by administration of either Ramipril or Hoe140. In the heart, the intercapillary distance was significantly higher in SNX, but it was not lowered by either early or late Ramipril or Hoe140 treatment. Treatment of SNX with Hoe140 alone, however, resulted in a marked further increase in intercapillary distance. The wall thickness of the aorta was significantly higher in SNX than in controls; early and late Ramipril treatment prevented such increase, and this effect was antagonized by Hoe140. CONCLUSION: These findings illustrate that bradykinin plays an important role for the beneficial effect of Ramipril in preventing (and potentially reversing) abnormal cardiovascular structure in uremic hypertensive rats.     

Beneficial effects of chrysin on the reproductive system of adult male rats

In this study, the beneficial effect of chrysin, a natural flavonoid currently under investigation due to its important biological activities, on reproductive system of rats was investigated. Rats (n = 16) were divided randomly into two equal groups. Rats in control group were given corn oil as carrier. Chrysin was orally administered at the dose of 50 mg kg(-1) per day by gavages, and it was dissolved in corn oil for 60 days. Tissue thiobarbituric acid reactive substances (TBARS) and glutathione (GSH) levels, antioxidant enzyme activity (CAT, SOD and GSH-Px), sperm parameters (motility, concentration and abnormal sperm rate), reproductive organ weight (testes, epididymis, vesicula seminalis, prostate) and serum testosterone levels were determined in the rats. Our results indicated that chrysin significantly increased GSH, CAT, GSH-Px and CuZn-SOD levels, but did not change the formation of TBARS significantly. In addition, sperm motility, sperm concentration and serum testosterone levels significantly increased, whereas abnormal sperm rate significantly decreased with chrysin treatment. In conclusion, it is suggested that treatment with chrysin can positively affect the reproductive system in rats, and it can be used for the treatment of male infertility.     

Suppression of experimental abdominal aortic aneurysms in the rat by treatment with angiotensin-converting enzyme inhibitors

PURPOSE: Pathologic remodeling of the extracellular matrix is a critical mechanism in the development and progression of abdominal aortic aneurysms (AAAs). Although angiotensin-converting enzyme (ACE) inhibitors are known to alter vascular wall remodeling in other conditions, their effects on AAAs are unknown. In this study we assessed the effect of ACE inhibitors in a rodent model of aneurysm development. METHODS: Male Wistar rats underwent transient aortic perfusion with porcine pancreatic elastase, followed by treatment with one of three ACE inhibitors (captopril [CP], lisinopril [LP], or enalapril [EP]), an angiotensin (AT)1 receptor antagonist (losartan [LOS]), or water alone (9 rats in each group). Blood pressure and aortic diameter (AD) were measured before elastase perfusion and on day 14, with an AAA defined as an increase in AD (DeltaAD) of more than 100%. The structural features of the aortic wall were examined by means of light microscopy. RESULTS: Aneurysmal dilatation consistently developed within 14 days of elastase perfusion in untreated rats, coinciding with the development of a transmural inflammatory response and destruction of the elastic media (mean DeltaAD, 223% +/- 28%). All three ACE inhibitors prevented AAA development (mean DeltaAD: CP, 67% +/- 4%; LP, 18% +/- 12%; and EP, 14% +/- 3%; each P <.05 vs controls). ACE inhibitors also attenuated the degradation of medial elastin without diminishing the inflammatory response. Surprisingly, the aneurysm-suppressing effects of ACE inhibitors were dissociated from their effects on systemic hemodynamics, and LOS had no significant effect on aneurysm development compared with untreated controls (mean DeltaAD, 186% +/- 19%). CONCLUSION: Treatment with ACE inhibitors suppresses the development of elastase-induced AAAs in the rat. Although this is associated with the preservation of medial elastin, the mechanisms underlying these effects appear to be distinct from hemodynamic alterations alone or events mediated solely by AT1 receptors. Further studies are needed to elucidate how ACE inhibitors influence aortic wall matrix remodeling during aneurysmal degeneration.     

De-novo expression of vascular ecto-5′-nucleotidase and down-regulation of glomerular ecto-ATPase in experimental chronic renal transplant failure

Ischemic injury plays an important role in chronic renal transplant failure (CRTF). Down-regulation of ecto-adenosine triphosphatase (ATPase) in combination with up-regulation of ecto-5'-nucleotidase is a hallmark of ischemic injury. We studied the expression of renal ecto-5'-nucleotidase and ecto-ATPase in experimental renal transplantation. Fisher 344-to-Lewis allografted rats were either treated with an angiotensin-converting enzyme inhibitor (ACEi) or left untreated. Lewis-to-Lewis syngrafted rats served as controls. Untreated allografted rats developed proteinuria, glomerulosclerosis, and mild intimal hyperplasia. ACEi completely prevented focal and segmental glomerulosclerosis (FGS) and proteinuria, but significantly enhanced intimal hyperplasia. Untreated allografted rats revealed marked vascular ecto-5'-nucleotidase activity, which increased with ACEi. Vascular ecto-5'-nucleotidase activity was absent in syngrafted animals. Ecto-5'-nucleotidase activity correlated well with intimal hyperplasia. Glomerular ecto-ATPase expression was significantly reduced in untreated allografted rats compared to syngrafted rats and correlated well with the extent of FGS. ACEi prevented reduction in glomerular ecto-ATPase. We found de-novo expression of ecto-5'-nucleotidase at sites of renal intimal hyperplasia. Glomerular ecto-ATPase expression was markedly reduced in allografted rats and was prevented by ACEi. These enzyme expression patterns suggest local ischemic damage in experimental CRTF.     

6‐Gingerol‐rich fraction prevents disruption of histomorphometry and marker enzymes of testicular function in carbendazim‐treated rats

Previous investigations demonstrated that 6‐gingerol‐rich fraction (6‐GRF) prevented testicular toxicity via inhibition of oxidative stress and endocrine disruption in CBZ‐treated rats. The influence of 6‐GRF on alterations in histomorphometry and marker enzymes of testicular function in CBZ‐treated rats which hitherto has not been reported was investigated in this study. The animals were orally administered either CBZ (50 mg/kg) alone or in combination with 6‐GRF (50, 100 and 200 mg/kg) for 14 consecutive days. Histomorphormetric analysis demonstrated that 6‐GRF significantly prevented CBZ‐mediated increase in the organo‐somatic index of the testes and seminiferous tubular diameter as well as the reduction in epithelium height and tubular length of testes in the rats. Similarly, 6‐GRF ameliorated CBZ‐induced disruption in the epithelium height as well as in the proportion of tubule and interstitium of the epididymis the treated rats. Furthermore, 6‐GRF prevented CBZ‐mediated increase in testicular acid phosphatase activity and the decrease in testicular alkaline phosphatase, aminotransferases, glucose‐6‐phosphate dehydrogenase and lactate dehydrogenase activities. Moreover, 6‐GRF ameliorated CBZ‐induced reduction in the testicular and epididymal sperm count and sperm motility in the treated rats. Conclusively, 6‐GRF enhances key functional enzymes involve in spermatogenesis and maintains histo‐architecture of testes and epididymis in CBZ‐treated rats.     

Lung angiotensin converting enzyme activity in rats with differing susceptibilities to chronic hypoxia.

The decrease in lung angiotensin converting enzyme (ACE) activity occurring in rats during chronic hypoxia might be related to the pulmonary haemodynamic response or to the hypoxia. A study in rats was carried out to investigate this question. Rats from the Hilltop (H) strain are known to develop more severe pulmonary hypertension as a result of chronic hypoxia than rats from the Madison (M) strain despite having virtually identical arterial and mixed venous oxygen tensions. Rats from H and M strains were exposed to hypoxia (0.5 atm) for 3-21 days and lung and serum ACE activities were determined. After three days' hypobaria lung ACE activity was significantly lower and serum ACE significantly higher in H than in M rats. Linear regressions for lung ACE activity and right ventricular:body weight ratios showed significant inverse correlations and were similar in the two strains. The results suggest that pulmonary hypertension and not hypoxia determines the reduction in lung ACE activity, possibly by releasing ACE into the blood stream.