Djelovanje taurina protiv histomorfoloških i ultrastrukturnih promjena u testisima miševa izloženih aluminijevu kloridu

The aim of this study was to investigate the protective effects of taurine against histomorphological and ultrastructural changes in the testes of Swiss albino mice caused by acute in vivo exposure to AlCl3. Light microscopy revealed that a single intraperitoneal (i.p.) dose of AlCl3 (25 mg kg-1 Al3+) was associated with sloughing, tubular atrophy, germ-cell degeneration, and foci of Leydig cell hyperplasia. In addition, transmission electron microscopy showed a destruction of inter-Sertoli cell tight junctions, apoptotic cell death of spermatogonia and primary spermatocytes, various types of abnormalities in spermatid morphology, accumulation of lipid droplets, reduction of the smooth endoplasmic reticulum (sER), and mitochondrial damage in Leydig cells. Taurine post-treatment at i.p. dose of 1 g kg-1 diminished these changes and significantly reduced the number of affected tubules compared to Al-poisoned mice. This is the first study to evidence that taurine protects against pathological changes in the testicular tissue of Al-treated mice.promjena u testisima švicarskih albino miševa akutno izloženih AlCl3. Svjetlosnom je mikroskopijom utvrđena povezanost između jednokratne intraperitonealne (i.p.) doze AlCl3 (25 mg kg-1 Al3+) i odvajanja nekrotičnoga tkiva, atrofije tubula, degeneracije zametnih stanica te žarišta hiperplazije Leydigovih stanica. Usto su se elektronskom mikroskopijom mogli vidjeti razoreni čvrsti spojevi između Sertolijevih stanica, apoptoza spermatogonija i primarnih spermatocita, različite morfološke abnormalnosti spermatida, nakupljanje lipidnih kapi, stanjenje glatkog endoplazmatskog retikuluma (sER) te oštećenje mitohondrija u Leydigovim stanicama. Naknadna primjena taurina u i.p. dozi od 1 g kg-1 ublažila je ove promjene i značajno smanjila broj zahvaćenih tubula u odnosu na miševe otrovane aluminijem. Ovo je prvo istraživanje koje potvrđuje zaštitno djelovanje taurina protiv patoloških promjena na tkivu testisa miševa uzrokovanih aluminijem

A simple and reliable protocol for long-term culture of murine bone marrow stromal (mesenchymal) stem cells that retained their in vitro and in vivo stemness in long-term culture

Table S1. List of primers used for qRT-PCR. Table S2. Full osteogenic gene expression list (total 84 genes) by BMSCs-FS (p25) versus ST2 cells during osteoblast differentiation including all significant/non-significant pathways. (DOCX 20 kb

Nitric oxide levels in chronic liver disease patients with and without oesophageal varices

Introduction Patients with chronic liver disease ultimately progress to develop cirrhosis and portal hypertension. Recently it seems well established that nitric oxide disturbances play a key role in the pathogenesis of chronic liver disease and portal hypertension. The aim of this work was to clarify the correlation between chronic liver disease stages, liver function status, esophageal varices presence and nitric oxide disturbances. Subjects and methods All subjects (n = 120) in the present study were classified into; group I which included 15 age and sex matched healthy volunteers (taken as control), group II which included 20 patients with chronic active hepatitis, and group III which included 85 patients with hepatic cirrhosis. All subjects included were subjected to full clinical assessment, routine laboratory investigations, serum nitrate level determination using colorimetric method, abdominal ultrasonography and upper endoscopy. Results Increased serum nitrate level could not be detected in patients with chronic active hepatitis as well as those with early cirrhosis (Child’s class A). Progressive and significant increase of serum nitrate levels were detected in more advanced stages of cirrhosis (Child’s class B & C). The best non-invasive predictor for the presence of oesophageal varices was a combination of platelet count <150.000/mm3, splenomegaly >18 cm, Child’s class B or C and serum nitrate ≥38 μmol/l, with 93.3% sensitivity and 100% specificity. Conclusion Serum nitrate level can be used as a non-invasive predictor for progression of chronic liver disease as well as for the presence of oesophageal varices

Hemin Attenuates Cisplatin-Induced Acute Renal Injury in Male Rats

Background. The aim of this study is to investigate the protective effects of hemin (the heme oxygenase-1 [OH-1] inducer) against nephrotoxic effects induced by cisplatin [cis-diamminedichloroplatinum II (CP)] in male rats. Methods. The evaluation was performed through monitoring renal redox parameters: lipid peroxidation (LPO), glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione reductase (GR), and reduced glutathione (GSH). The work also examined renal function tests (urea and creatinine), tissue proinflammatory mediator like nitric oxide (NO), and kidney cytopathology. Results. A single intraperitoneal dose of CP (10 mg/kg b.w.) caused significant elevation of blood urea, serum creatinine, and renal LPO and NO, along with significant decline of the activities of GPx and GR, but renal SOD activity and GSH level were statistically insignificant as compared to control group. Subcutaneous injection of hemin (40 µmol/kg b.w.) partially ameliorated CP-induced renal damage, based on suppression of blood urea, serum creatinine, the renal MDA and NO levels, and increased antioxidant capacity in CP-treated rats. The results of histopathological and ultrastructural investigations supported the renoprotective effect of hemin against CP-induced acute toxicity. Conclusion. The induction of HO-1 by hemin is a promising approach in the treatment of CP-induced nephrotoxicity. However, further preclinical studies are warranted to test effectiveness of CP/hemin on the outcome of tumor chemotherapy

Rutin ameliorates carbon tetrachloride (CCl4)-induced hepatorenal toxicity and hypogonadism in male rats

Rutin, a food derived-polyphenolic bioflavonoid, has been acknowledged for several health benefits. This study aims to explore the ameliorative effects of rutin against carbon tetrachloride (CCl4) toxicity in male rats. Adult male rats were given either CCl4 (30% in olive oil, 3 ml/kg b.w. intraperitoneally) alone or in combination with rutin (70 mg/kg intragastrically) twice a week for 4 weeks. Our data showed that rutin mitigated CCl4 hepatorenal damage, as indicated by diagnostic markers (i.e., transaminases, alkaline phosphatase, total bilirubin, total protein, albumin, urea, uric acid and creatinine), and histopathological findings. In addition, CCl4 induced profound elevation of free radical generation and oxidative stress, as evidenced by increasing lipid peroxidation and reducing catalase, superoxide dismutase and glutathione peroxidase activities in liver, kidney and testicular tissues; these effects were suppressed by coexposure with rutin. Moreover, the increase in the levels of serum triglycerides, cholesterol, low-density lipoprotein cholesterol, and very-low-density lipoprotein cholesterol induced by CCl4 was effectively counteracted by rutin. The decrease in the level of high-density lipoprotein cholesterol in the CCl4 group was also counteracted by rutin treatment. Interestingly, the decreased levels of hormonal mediators associated with sperm production, including serum testosterone, luteinizing hormone and follicle-stimulating hormone, and the impaired sperm quality induced by CCl4 were reversed by rutin. Data from the current study clearly demonstrated that rutin supplementation could at least partly overcome CCl4-induced hepatotoxicity, nephrotoxicity and reproductive toxicity by antioxidant and antidyslipidemic effects

Ultrastructure changes in hepatocytes of catfish Clarias gariepinus from Lake Mariut, Egypt

Abstract: In the present study, specimens of catfish (Clariidae) were collected from a polluted location (Main Basin) and a relatively clean area (East Basin) in Lake Mariut, one of the Nile Delta Lakes in Egypt. Fifteen fish were taken from each site. Liver preparations of fish from the two sources were comparatively examined for cellular changes using transmission electron microscopy. Fish hepatocytes from the polluted area showed accumulation of the heterochromatin, enlarged nucleoli, and an extremely folded nuclear envelope. Perichromatin granules were increased and progressively formed small clusters closely associated with patches of heterochromatin. In the cytoplasm, fractionation, dilation, and vesiculation of rough endoplasmic reticulum (RER), and elevated amounts of smooth endoplasmic reticulum (SER) tubules were noted. The most frequent pathological modifications were the swelling of mitochondria, cristae regression and changes in the electron-transparency of the matrix. Lysosomes showing myelin-like stacks of membraneous material (phospholipidosis), glycogenosomes (i.e., glycogen rosettes enclosed by membranes) and cytoplasmic myelinated bodies were strongly developed. Furthermore, increasing numbers of secondary lysosomes with degraded cell organelles were found. With reference to the storage vesicles, there appeared to be an increase in the lipid droplets (lipidosis) within many hepatocytes. This study reinforces the need to select representative sentinel species from different habitats for biomonitoring purposes and it provides further support for the use of biomarkers in assessing the health of aquatic ecosystems

The influence of taurine pretreatment on aluminum chloride induced nephrotoxicity in Swiss albino mice

The present study was carried out to investigate (1) the alterations in biochemical parameters, free radicals and enzyme activities induced by aluminum chloride (AlCl3) in kidney of male Swiss albino mice, and (2) the role of taurine in alleviating the nephrotoxic effects of AlCl3. Taurine plays an important role as an antioxidant and is consequently expected to protect tissues from damage caused by reactive oxygen metabolites. The animals were randomized into four groups (n=6/group). Group I was the control group. Group II received a single dose of AlCl3 (25 mg Al3+/kg b.w., ip). Group III received taurine (100 mg/kg b.w., ip) for 5 consecutive days before administration of AlCl3 (25 mg Al3+/kg b.w., ip). Group IV received taurine (100 mg/kg b.w., ip) for 5 consecutive days. 24 h following the administration of compounds, all the mice were assessed using serum and tissue homogenate biomarkers as well as the pathological evaluation. Exposure to AlCl3 led to an increased level of renal lipid peroxidation as measured by malondialdehyde (MDA), while reduced glutathione (GSH), glutathione peroxidase (GPx) and catalase (CAT) decreased. Marked elevation of blood urea and serum creatinine concentrations were also observed in AlCl3 treated mice, thereby indicating renal damage. All these factors were significantly improved by taurine pretreatment. The histological and ultrastructural observations on the kidney tissues also confirmed the renoprotective nature of taurine. Thus these results may indicate that taurine treatment protects against functional, biochemical and morphological damage in AlCl3-induced acute renal failure in mice

Photomicrographs of rat liver (H&E stain).

<p><b>(A)</b> Control liver showing normal hepatocytes arranged in cords, obvious sinusoids (s), and central vein (cv). <b>(B, C)</b> Hepatic injury induced by CCl₄. Note hepatic cells with ballooning degeneration (b), focal necrotic cell death (ne), and diffuse fatty changes (arrows) (in B). Microvesicular steatosis (i.e., accumulation of small fat droplets) in hepatocyte cytosol (arrows), and inflammatory infiltrates (arrowhead) are evident in liver tissue (in C). <b>(D)</b> CCl₄+TAU group showing an improvement of cellular structure and uniform sinusoidal arrays (compared to B). Pathological fatty deposition (arrows) and also normal centrilobular hepatocytes (h) with well-defined cell borders, dense cytoplasm and central nuclei are visible. <b>(E)</b> CCl₄+SIL group with less severe liver injury. Focal hepatocellular degeneration (d) is observed. <b>(F)</b> CCl₄+TAU+SIL group indicating no pathologic lesions.</p