On the toxicity of gold nanoparticles: Histological, histochemical and ultrastructural alterations.

Gold nanoparticles (Au NPs) are used in diagnostic and therapeutic applications together with a variety of industrial purposes and in many biomedical sectors with potential risks to human health. The present study aimed to the histological, histochemical, and ultrastructural alterations induced by Au NPS in vital organs. Healthy male Wistar Albino rats (Rattus norvegicus) were subjected to 20 injections of 10-nm Au NPs at a daily dose of 2 mg/kg. Liver, kidney, heart, and lung biopsies from control and Au NPs-treated rats under study were subjected to histological and histochemical examinations. In comparison with the control rats, the renal tissue of Au NPs-treated rats demonstrated glomerular congestion, interstitial inflammatory cell infiltration, renal tubular hydropic degeneration, cloudy swelling, necrosis, and hyaline cast precipitation. In addition, Au NPs induced the following hepatic alterations: hepatocyte cytolysis, cytoplasmic vacuolation, hydropic degeneration, and nuclear alterations together with sinusoidal dilatation. Moreover, the hearts of the treated rats demonstrated myocarditis, cardiac congestion, hyalinosis, cardiomyocyte hydropic degeneration, myofiber disarray and cardiac congestion. The lungs of Au NPs-treated rats also exhibited the following pulmonary alterations: alectasis, emphysema, inflammatory cell inflammation, thickened alveolar walls, pulmonary interstitial edema, congestion, hypersensitivity, fibrocyte proliferation, and honeycombing. In conclusion, exposure to Au NPs induced histological, histochemical and ultrastructural alterations in the vital organs that may alter the function of these organs. Additional efforts are needed for better understanding the potential risks of Au NPs to human health.

Renal histological alterations induced by acute exposure of titanium dioxide nanoparticles / Alteraciones histológicas renales inducidas por la exposición aguda de nanopartículas de dióxido de titanio

SUMMARY: Titanium dioxide nanoparticles (TiO2 NPs) are widely used in many commercial products, nanomedicine, agriculture, personal care products, different industries and pharmaceutical preparations with potential risk in human health and the environment. The current work was conducted to investigate the renal damage that might be induced by the acute toxicity TiO2 NPs. A total of 40 healthy male adult Wistar albino rats (Rattus norvegicus) were exposed to TiO2 NPs (126, 252, 378 mg/kg bw) for 24 and 48 h. Fresh portions of the kidneys from each rat were processed for histological and histochemical alterations. In comparison with respective control rats, exposure to TiO2 NPs has marked the following glomerular, tubular and interstitial alterations including the followings: glomerular congestion, Bowman's capsule swelling and dilatation, inflamed glomeruli, renal tubules cloudy swelling, karyorrhexis, karyolysis, infiltration of inflammatory cells, congestion, necrosis, hydropic degeneration, dilatation and congestion of blood vessels, hyaline droplets and hyaline casts precipitation, interstitial edema and fibrosis. From the findings of the current work one may conclude that TiO2 NPs are capable of inducing kidney damage with more insulation in the cortex and the proximal convoluted tubules than the medulla and the distal ones respectively. In addition, it might be concluded that renal damage induced by these nanomaterials is dose and duration of exposure dependent. Further hematological, biochemical, immunohistochemical, and ultra-structural studies are recommended.

RESUMEN: Las nanopartículas de dióxido de titanio (TiO2 NP) se usan ampliamente en muchos productos comerciales, nanomedicina, agricultura, productos para el cuidado personal, diferentes industrias y preparaciones farmacéuticas con riesgo potencial para la salud humana y el medio ambiente. El trabajo actual se realizó para investigar el daño renal que podría ser inducido por la toxicidad aguda NP de TiO2. Un total de 40 ratas Wistar albinas adultas sanas (Rattus norvegicus) fueron expuestas a TiO2 NP (126, 252, 378 mg / kg de peso corporal) durante 24 y 48 h. Las muestras de los riñones de las ratas se procesaron para estudios histológicos e histoquímicos. En comparación con las ratas control, la exposición de las ratas a TiO2 NP presentaron las siguientes alteraciones glomerulares, tubulares e intersticiales: congestión glomerular, dilatación de la cápsula de Bowman, inflamación glomerular, túbulos renales aumentados, cariorrexis, cariólisis, infiltración de células inflamatorias, congestión, necrosis, degeneración hidrópica, dilatación y congestión de vasos sanguíneos, gotas y precipitaciones hialina, edema intersticial y fibrosis. A partir de los hallazgos del trabajo actual, se puede concluir que las NP de TiO 2 son capaces de inducir daño renal con más aislamiento en la corteza y en los túbulos contorneados proximales que en la médula y los túbulos contorneados distales, respectivamente. Además, se podría concluir que el daño renal inducido por estos nanomateriales depende de la dosis y la duración de la exposición. Se recomiendan estudios adicionales hematológicos, bioquímicos, inmunohistoquímicos y ultraestructurales.

In vivo investigation on the chronic hepatotoxicity induced by sertraline.

Although sertraline is widely prescribed as relatively safe antidepressant drug, hepatic toxicity was reported in some patients with sertraline treatment. The present study was conducted to investigate the morphometric, hepatotoxicity, and change in gene expression of drug metabolizing enzymes. Male healthy adult rabbits (Oryctolagus cuniculus) ranging from 1050 to 1100 g were exposed to oral daily doses of sertraline (0, 1, 2, 4, 8 mg/kg) for 9 weeks. The animals were subjected to morphometric, hepatohistological, histochemical and quantitative real-time polymerase chain reaction analyses. Sertraline chronic exposure induced morphometric changes and provoked histological and histochemical alterations including: hepatocytes hydropic degeneration, necrosis, nuclear alteration, sinusoidal dilation, bile duct hyperplasia, inflammatory cells infiltration, portal vessel congestion, Kupffer cells hyperplasia, portal fibrosis and glycogen depletion. In addition, the gene expression of drug and arachidonic acid metabolizing enzymes were reduced significantly (p value <0.05). The most affected genes were cyp4a12, ephx2, cyp2d9 and cyp1a2, demonstrating 5 folds or more down-regulation. These findings suggest that chronic sertraline treatment induced toxic histological alterations in the hepatic tissues and reduced the gene expression of drug metabolizing enzymes. Patients on chronic sertraline treatment may be on risk of hepatotoxicity with reduced capacity to metabolize drugs and fatty acids.

Ameliorative effect of propolis against hepatorenal alterations induced by methotrexate: morphohistopathological study / Efecto protector del propóleo en las alteraciones hepatorrenales inducidas por el metotrexato: estudio morfohistopatológico

Methotrexate (MTX) is widely used in the treatment of some forms of cancer but having severe side effects. The present work aimed to investigate the protective role of propolis treatment against alterations induced by MTX on the hepatic and renal tissues. Rabbits were exposed to MTX (0.25 mg/kg), with or without propolis (50 mg/kg) while hepatic and renal biopsies were examined for histological and histochemical abnormalities. Methotrexate induced hydropic degeneration, pyknosis, sinusoidal dilatation and bile duct hyperplasia in the liver together with renal tubular degeneration, glomerular shrinkage and hyaline droplet precipitation. While propolis partially ameliorated some of the morphometric and biochemical alterations, none of the hepatic alterations induced by MTX was protected by propolis treatment. Nevertheless glomerular shrinkage and renal tubule degeneration were partially protected in animals received both MTX plus propolis. It is concluded that propolis treatment has little or no ameliorative effect in protecting the hepatic and renal tissues from MTX toxicity.

El metotrexato (MTX) es ampliamente utilizado en el tratamiento de algunas formas de cáncer, pero tiene efectos secundarios graves. El presente trabajo tuvo como objetivo investigar el papel protector del tratamiento con própoleo frente a las alteraciones inducidas por el MTX en los tejidos hepático y renal. Se expusieron conejos a MTX (0,25 mg / kg), en grupos con y sin propóleo (50 mg / kg), y se realizaron biopsias hepáticas y renales, que fueron examinadas buscando anomalías histológicas e histoquímicas. El metotrexato indujo la degeneración hidrópica, picnosis, dilatación sinusoidal e hiperplasia del conducto biliar en el hígado, junto con la degeneración tubular renal, la contracción glomerular y la precipitación hialina. Mientras que el propóleo parcialmente mejoró algunas de las alteraciones morfométricas y bioquímicas, ninguna de las alteraciones hepáticas inducidas por MTX fue protegido por el tratamiento con propóleo. Sin embargo, la contracción glomerular y la degeneración de los túbulos renales fueron parcialmente protegidos en animales que recibieron MTX más propóleo. Se concluye que el tratamiento con propóleo tiene poco o ningún efecto mejorador en la protección de los tejidos hepáticos y renales sometidos a la toxicidad de MTX.

Zinc oxide nanoparticles hepatotoxicity: Histological and histochemical study.

Zinc oxide nanoparticles (ZnO NPs) are widely used in industry and cosmetic products with promising investment in medical diagnosis and treatment. However, these particles may reveal a high potential risk for human health with no information about hepatotoxicity that might be associated with their exposure. The present work was carried out to investigate the histological and histochemical alterations induced in the hepatic tissues by naked 35nm ZnO NPs. Male Wistar albino rats were exposed to ZnO NPs at a daily dose of 2mg/kg for 21days. Liver biopsies from all rats under study were subjected to histopathological examinations. In comparison with the control rats, the following histological and histochemical alterations were demonstrated in the hepatic tissues of rats exposed to ZnO NPs: sinusoidal dilatation, Kupffer cells hyperplasia, lobular and portal triads inflammatory cells infiltration, necrosis, hydropic degeneration, hepatocytes apoptosis, anisokaryosis, karyolysis, nuclear membrane irregularity, glycogen content depletion and hemosidrosis. The findings of the present work might indicate that ZnO NPs have potential oxidative stress in the hepatic tissues that may affect the function of the liver. More work is needed to elucidate the toxicity and pathogenesis of zinc oxide nanoparticles on the vital organs.

Ultrastructural hepatocytic alterations induced by silver nanoparticle toxicity.

Silver nanoparticles (SNPs) are widely used in nanomedicine and consuming products with potential risk to human health. While considerable work was carried out on the molecular, biochemical, and physiological alterations induced by these particles, little is known of the ultrastructural pathological alterations that might be induced by nanosilver materials. The aim of the present work is to investigate the hepatocyte ultrastructural alterations that might be induced by SNP exposure. Male rats were subjected to a daily single dose (2 mg/kg) of SNPs (15-35 nm diameter) for 21 days. Liver biopsies from all rats under study were processed for transmission electron microscopy examination. The following hepatic ultrastructural alterations were demonstrated: mitochondria swelling and crystolysis, endoplasmic reticulum disruption, cytoplasmic vacuolization, lipid droplets accumulation, glycogen depletion, karyopyknosis, apoptosis, sinusoidal dilatation, Kupffer cells activation, and myelin figures formation. The current findings may indicate that SNPs can induce hepatocyte organelles alteration, leading to cellular damage that may affect the function of the liver. These findings might indicate that SNPs potentially trigger heptocyte ultrastructural alterations that may affect the function of the liver with potential risk on human health in relation to numerous applications of these particles. More work is needed to elucidate probable ultrastructural alterations in the vital organs that might result from nanosilver toxicity.

Histological alterations in the liver of rats induced by different gold nanoparticle sizes, doses and exposure duration.

BACKGROUND: Nanoparticles (NPs) can potentially cause adverse effects on organ, tissue, cellular, subcellular and protein levels due to their unusual physicochemical properties. Advances in nanotechnology have identified promising candidates for many biological and biomedical applications. Since the properties of NPs differ from that of their bulk materials, they are being increasingly exploited for medical uses and other industrial applications. The aim of the present study was to investigate the particle-size effect of gold nanoparticles (GNPs) on the hepatic tissue in an attempt to cover and understand the toxicity and the potential threat of their therapeutic and diagnostic use. METHODS: To investigate particle-size effect of GNPs on the hepatic tissue, a total of 70 healthy male Wistar-Kyoto rats were exposed to GNPs received 50 or 100 ul of GNPs infusion of size (10, 20 and 50 nm for 3 or 7 days). RESULTS: In comparison with respective control rats, exposure to GNPs doses has produced alterations in the hepatocytes, portal triads and the sinusoids. The alterations in the hepatocytes were mainly summarized as hydropic degeneration, cloudy swelling, fatty degeneration, portal and lobular infiltrate by chronic inflammatory cells and congestive dilated central veins. CONCLUSIONS: The induced histological alterations might be an indication of injured hepatocytes due to GNPs toxicity that became unable to deal with the accumulated residues resulting from metabolic and structural disturbances caused by these NPs. These alterations were size-dependent with smaller ones induced the most effects and related with time exposure of GNPs. The appearance of hepatocytes cytoplasmic degeneration and nuclear destruction may suggest that GNPs interact with proteins and enzymes of the hepatic tissue interfering with the antioxidant defense mechanism and leading to reactive oxygen species (ROS) generation which in turn may induce stress in the hepatocytes to undergo atrophy and necrosis. More histomorphologcal, histochemical and ultrastrucural investigations are needed in relation of the application of GNPs with their potential threat as a therapeutic and diagnostic tool.

Histological and histochemical alterations in the liver induced by lead chronic toxicity.

Adult males of the Wistar albino rats (Rattus norvegicus) were exposed to lead acetate trihydrate in drinking water (0.0%, 0.25%, 0.5%, 1% and 2% for 1-12 months) to investigate histological and histochemical alterations induced by lead intoxication in the liver. Chronic exposure to subtoxic concentrations of lead produced changes in the hepatocytes, portal triads and the sinusoids. The alterations in the hepatocytes were mainly anisokaryosis, nuclear vesiculation, binucleation, cytoplasmic inclusions, cytoplasmic swelling, hydropic degeneration, necrosis and reduction in glycogen content. In addition, portal triads mild chronic inflammation, Kupffer cells hyperplasia and occasional fatty change were seen together with hemosiderosis. No portal fibrosis or cirrhosis was detected due to chronic subtoxic doses of lead exposure in the liver of any member of the dose groups over the entire period of the study. Chronic lead exposure also increased the activities of alkaline phosphatase and α-glycerophosphate-dehydrogenase which might be an adaptation to the metabolic, structural and functional changes in the organelles of hepatic cells due to lead intoxication. The findings revealed that chronic exposure to lead produced significant histological and histochemical changes in the liver of the Wistar albino rats.

Chemical composition of gallstones from Al-jouf province of saudi arabia.

BACKGROUND: It is essential to understand the aetiopathogenesis of gallstone disease. This study was undertaken to determine the chemical composition of gallstones from patients living in Al-Jouf Province of Saudi Arabia. METHODS: This was a descriptive study where 46 gallstones from Al-Jouf Province of Saudi Arabia were analysed by semiquantitative titrimetric and colourimetric methods. The proportion of different types of gallstones was described using 95% confidence interval based on exact method. RESULTS: Gallstones were found more frequently in female patients (60.9%) than males (39.1%), and these stones were composed of pure cholesterol (54.3%), pure bilirubin (2.2%), or mixed stones (43.5%). The most common chemical constituent was cholesterol (82.6%), while bilirubin was seen in 26.1% of the stones. Calcium was present in 32.6% of the stones in the form of calcium salts of bilirubin and carbonate. Bilirubin-containing stones were slightly more frequent in males than in females, while cholesterol-containing stones were less frequent in males. CONCLUSION: The findings indicate that gallstones in the Al-Jouf Province develop more frequently in the age group of the third decade of life, with more risk among females than males, and are predominated by cholesterol together with calcium bilirubinate and calcium carbonate.

Renal tissue alterations were size-dependent with smaller ones induced more effects and related with time exposure of gold nanoparticles.

BACKGROUND: Gold nanoparticles (GNPs) have important application for cell labeling and imaging, drug delivery, diagnostic and therapeutic purposes mainly in cancer. Nanoparticles (NPs) are being increasingly exploited for medical applications. The aim of the present study was to investigate the particle-size and period effects of administration of GNPs on the renal tissue in an attempt to address their potential toxicity. METHODS: A total of 70 healthy male Wistar-Kyoto rats were exposed to GNPs received 50 or 100 µl of GNPs infusion of size (10, 20 and 50 nm for 3 or 7 days) to investigate particle-size effect of GNPs on the renal tissue. Animals were randomly divided into groups, 6 GNPs-treated rats groups and one control group. Groups 1, 2 and 3 received infusion of 50 µl GNPs of size 10 nm (3 or 7 days), size 20 nm (3 or 7 days) and 50 nm (3 or 7 days), respectively; while groups 4, 5 and 6 received infusion of 100 µl GNPs of size 10 nm, size 20 nm and 50 nm, respectively. Stained sections of control and treated rats kidneys were examined for renal tissue alterations induced by GNPs. RESULTS: In comparison with respective control rats, exposure to GNPs doses has produced the following renal tubular alterations: cloudy swelling, vacuolar degeneration, hyaline droplets and casts, anisokaryosis, karopyknosis, karyorrhexis and karyolysis. The glomeruli showed moderate congestion with no hypercelluraity, mesangial proliferation or basement membrane thickening. The histological alterations were mainly seen in the cortex and the proximal renal convoluted tubules were more affected than the distal ones. CONCLUSIONS: The induced histological alterations might be an indication of injured renal tubules due to GNPs toxicity that became unable to deal with the accumulated residues resulting from metabolic and structural disturbances caused by these NPs. The findings may suggest that GNPs interact with proteins and enzymes of the renal tissue interfering with the antioxidant defense mechanism and leading to reactive oxygen species (ROS) generation which in turn may induce stress in the renal cells to undergo atrophy and necrosis. The produced alterations were size-dependent with smaller ones induced more affects and related with time exposure of GNPs.

Gold nanoparticles induced cloudy swelling to hydropic degeneration, cytoplasmic hyaline vacuolation, polymorphism, binucleation, karyopyknosis, karyolysis, karyorrhexis and necrosis in the liver.

BACKGROUND: Nanoparticles (NPs) can potentially cause adverse effects on organ, tissue, cellular, subcellular and protein levels due to their unusual physicochemical properties. Advances in nanotechnology have identified promising candidates for many biological and biomedical applications. The aim of the present study was to investigate the particle-size, dose and exposure duration effects of gold nanoparticles (GNPs) on the hepatic tissue in an attempt to cover and understand the toxicity and their potential therapeutic and diagnostic use. METHODS: A total of 70 healthy male Wistar-Kyoto rats were exposed to GNPs received 50 or 100 ul of GNPs infusion of size (10, 20 and 50 nm for 3 or 7 days) to investigate particle-size, dose and exposure duration effects of GNPs on the hepatic tissue. RESULTS: In comparison with respective control rats, exposure to GNPs doses has produced alterations in the hepatocytes, portal triads and the sinusoids. The alterations in the hepatocytes were mainly vacuolar to hydropic degeneration, cytopasmic hyaline vacuolation, polymorphism, binucleation, karyopyknosis, karyolysis, karyorrhexis and necrosis. CONCLUSIONS: The hepatocytes swelling might be exhibited as a result of disturbances of membranes function that lead to massive influx of water and Na+ due to GNPs effects accompanied by leakage of lysosomal hydrolytic enzymes that lead to cytoplasmic degeneration and macromolecular crowding. Hydropic degeneration is a result of ion and fluid homestasis that lead to an increase of intracellular water. The vacuolated swelling of the cytoplasm of the hepatocytes of the GNPs treated rats might indicate acute and subacute liver injury induced by the GNPs. Binucleation represents a consequence of cell injury and is a sort of chromosomes hyperplasia which is usually seen in regenerating cells. The induced histological alterations might be an indication of injured hepatocytes due to GNPs toxicity that became unable to deal with the accumulated residues resulting from metabolic and structural disturbances caused by these NPs. These alterations were size-dependent with smaller ones induced the most effects and related with time exposure of GNPs. The appearance of hepatocytes cytoplasmic degeneration and nuclear destruction may suggest that GNPs interact with proteins and enzymes of the hepatic tissue interfering with the antioxidant defense mechanism and leading to reactive oxygen species (ROS) generation which in turn may induce stress in the hepatocytes to undergo atrophy and necrosis. More histomorphologcal, histochemical and ultrastrucural investigations are needed in relation of the application of GNPs with their potential role as a therapeutic and diagnostic tool.

Gold nanoparticles administration induced prominent inflammatory, central vein intima disruption, fatty change and Kupffer cells hyperplasia.

BACKGROUND: Advances in nanotechnology have identified promising candidates for many biological, biomedical and biomedicine applications. They are being increasingly exploited for medical uses and other industrial applications. The aim of the present study was to investigate the effects of administration of gold nanoparticles (GNPs) on inflammatory cells infiltration, central vein intima disruption, fatty change, and Kupffer cells hyperplasia in the hepatic tissue in an attempt to cover and understand the toxicity and the potential threat of their therapeutic and diagnostic use. METHODS: A total of 70 healthy male Wistar-Kyoto rats were exposed to GNPs received 50 or 100 µl of GNPs infusion of 10, 20 and 50 nm GNPs for 3 or 7 days. Animals were randomly divided into groups, 12 GNPs-treated rats groups and one control group (NG). Groups 1, 2 and 3 received infusion of 50 µl GNPs of size 10 nm (3 or 7 days), size 20 nm (3 or 7 days) and 50 nm (3 or 7 days), respectively; while groups 4, 5 and 6 received infusion of 100 µl GNPs of size 10 nm, size 20 nm and 50 nm, respectively. RESULTS: In comparison with respective control rats, exposure to GNPs doses has produced alterations in the hepatocytes, portal triads and sinusoids. The alterations in the hepatocytes were mainly vacuolar to hydropic degeneration, cytopasmic hyaline vacuolation, polymorphism, binucleation, karyopyknosis, karyolysis, karyorrhexis and necrosis. In addition, inflammatory cell infiltration, Kupffer cells hyperplasia, central veins intima disruption, hepatic strands dilatation and occasional fatty change together with a loss of normal architechiture of hepatic strands were also seen. CONCLUSIONS: The alterations induced by the administration of GNPs were size-dependent with smaller ones induced more affects and related with time exposure of GNPs. These alterations might be an indication of injured hepatocytes due to GNPs toxicity that became unable to deal with the accumulated residues resulting from metabolic and structural disturbances caused by these NPs. These histological alterations may suggest that GNPs interact with proteins and enzymes of the hepatic tissue interfering with the antioxidant defense mechanism and leading to reactive oxygen species (ROS) generation which in turn may induce stress in the hepatocytes to undergo necrosis.

The appearance of renal cells cytoplasmic degeneration and nuclear destruction might be an indication of GNPs toxicity.

BACKGROUND: Advances in nanotechnology have identified promising candidates for many biological and biomedical applications. Since the properties of nanoparticles (NPs) differ from that of their bulk materials, they are being increasingly exploited for medical uses and other industrial applications. The histological and the histochemical alterations in the renal tissues due to gold nanoparticles (GNPs) have not well documented and have not yet been identified. The aim of the present study was to investigate the particle-size effect of GNPs on the renal tissue in an attempt to address their potential toxicity. METHODS: A total of 70 healthy male Wistar-Kyoto rats were exposed to GNPs received 50 or 100 µl of GNPs infusion of size (10, 20 and 50 nm for 3 or 7 days) to investigate particle-size effect of GNPs on the renal tissue. Animals were randomly divided into groups, 6 GNPs-treated rats groups and one control group. Groups 1, 2 and 3 received infusion of 50 µl GNPs of size 10 nm (3 or 7 days), size 20 nm (3 or 7 days) and 50 nm (3 or 7 days), respectively; while groups 4, 5 and 6 received infusion of 100 µl GNPs of size 10 nm, size 20 nm and 50 nm, respectively. RESULTS: The histological alterations were mainly seen in the cortex and the proximal renal convoluted tubules were more affected than the distal ones. In comparison with respective control rats, exposure to GNPs doses has produced the following renal tubular alterations: cloudy swelling and renal tubular necrosis. Interstitial alterations included: intertubular blood capillaries dilatation, intertubular hemorrhage and inflammatory cell infiltrations. The glomeruli showed moderate congestion with no hypercelluraity and mesangial proliferation or basement membrane thickening. CONCLUSIONS: The induced histological alterations might be an indication of injured renal tubules due to GNPs toxicity that become unable to deal with the accumulated residues resulting from metabolic and structural disturbances caused by these NPs. These alterations were size-dependent with smaller ones induced more effects and related with time exposure of GNPs. The produced histological alterations may suggest that GNPs interact with proteins and enzymes of the renal tissue interfering with the antioxidant defense mechanism and leading to reactive oxygen species (ROS) generation which in turn may induce stress in the renal cells to undergo atrophy and necrosis. More histomorphologcal investigations are needed to address the potential threat of GNPs as a therapeutic and diagnostic tool.

Histological alterations in the testicular tissue induced by sildenafil overdoses.

Twenty adult male rabbits (Oryctolagus cuniculus) received sildenafil (0, 1, 3, 6, 9 mg/kg/day) for 4 weeks to investigate the testicular histological alterations induced by overdoses of this drug. Exposure to overdoses of sildenafil had provoked tubular and interstitial histological alterations. Abnormality in the germinal epithelium of the seminiferous tubules included spermatocytes karyopyknosis, spermatocytes degeneration, desquamation, spermatid giant cells and arrest of spermatogenesis. Additionally, increased Leydig cells cellularity, tubular degeneration, thickening of the interstitium were also observed. The encountered histological findings indicate that chronic exposure to sildenafil overdoses produces significant morphological and histological alterations in the testes which finally might lead to complete arrest of spermatogenesis.

Histological alterations and biochemical changes in the liver of sheep following Echis coloratus envenomation.

Snake envenoming is a major problem in Al-Jouf Province of Saudi Arabia where most of these envenoming are caused by Echis coloratus which is the highest risk to human and animals in this Province. Little, if any, has been carried out on the histological alterations and biochemical changes in the liver of sheep following snake envenomation. Healthy adult male Ovis orientalis sheep were subjected to E. coloratus envenomation in an attempt to evaluate the histological alterations and biochemical changes in the liver. E. coloratus venom elevated glucose, aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglyceride and total bilirubin while cholesterol was reduced. The histological alterations were mainly pyknosis, karyorrhexis, cytoplasmic vacuolation, necrosis, fatty changes and hepatocytes atrophy. Sinusoidal dilatation, Kupffer cell activation, amyloidosis, portal vein thrombosis, partial glycogen depletion and hepatic architecture distortion were also detected. The findings revealed that E. coloratus venom produced biochemical changes and histological alterations in the liver of the envenomated sheep that might affect the functions of this organ severely.

Morphology: histology and histochemistry of the venom apparatus of the centipede, Scolopendra valida (Chilopoda, Scolopendridae) / Morfología, histología e histoquímica del aparato venenoso del ciempiés: Scolopendra valida (Chilopoda, Scolopendridae)

Morphological, histological and histochemical characterizations of the venom apparatus of the centapede, S. valida have been investigated. The venom apparatus of Scolopendra valida consists of a pair of maxillipedes and venom glands situated anteriorly in the prosoma on either side of the first segment of the body. Each venom gland is continuous with a hollow tubular claw possessing a sharp tip and subterminal pore located on the outer curvature. The glandular epithelium is folded and consists of a mass of secretory epithelium, covered by a sheath of striated muscles. The secretory epithelium consists of high columnar venom-producing cells having dense cytoplasmic venom granules. The glandular canal lacks musculature and is lined with chitinous internal layer and simple cuboidal epithelium. The histochemical results indicate that the venom-producing cells of both glands elaborate glycosaminoglycan, acid mucosubstances, certain amino acids and proteins, but are devoid of glycogen. The structure and secretions of centipede venom glands are discussed within the context of the present results.

Fueron investigadas las características morfológicas, histológicas e histoquímicas del aparato venenoso del ciempiés, S. valida. El aparato venenoso de Scolopendra valida consta de un par de maxilopodos y glándulas de veneno situadas anteriormente en el prosoma, a cada lado del primer segmento del cuerpo. Cada glándula de veneno se continúa en una garra con una cavidad tubular que posee una punta afilada y un poro subterminal situado sobre la curvatura externa. El epitelio glandular es plegado y se compone de una masa de epitelio secretor, cubierto por una vaina de los músculos estriados. El epitelio secretor consiste en células columnares altas productoras de veneno con gránulos citoplasmáticos de veneno densos. El conducto glandular carece de musculatura y está revestido por capa interna quitinosa y epitelio cuboidal simple. Los resultados histoquímicos indican que las células productoras de veneno de ambas glándulas elaboran glucosaminoglucanos mucosustancias ácidas, ciertos aminoácidos y proteínas, pero carecen de glucógeno. La estructura y las secreciones de las glándulas de veneno del ciempiés son examinadas en el contexto de los presentes resultados.

Epidemiological aspects of scorpion stings in Al-Jouf Province, Saudi Arabia.

BACKGROUND: Information on scorpion stings is available for many parts of Saudi Arabia, but not for Al-Jouf Province. METHODS: We reviewed and analyzed 1449 cases of scorpion stings that presented to the emergency department of the hospitals and medical centers in Al-Jouf Province during a 2-year period (2005-2006). RESULTS: The majority of patients (92.7%) manifested class I envenomation with local pain at the sting site as the primary complaint. Systemic toxicity was noticed in 7.3% of cases but no deaths were reported. Scorpion stings were recorded throughout the year with the highest seasonal incidence in the summer (64.3%) and the lowest during the winter (10.6%). The highest monthly incidence was in June (21.5%) and the lowest in December (1.5%). Most of the patients were male (77.3%) and the age of 44.2% of victims ranged between 15 to 30 years. Diurnal stings exceeded the nocturnal ones with a ratio of 3:2, and most of the stings were located mainly on the exposed limbs (88.6%), especially the lower limbs (51.7%). Leiurus quinquestriatus and Androctonus crassicauda were incriminated in most recorded cases. CONCLUSIONS: Our findings indicate that scorpion stings are common in Al-Jouf Province, especially during the summer. The overall threat to human health was found to be low.

Ultrastructural alterations in renal tissues of rabbits induced by diclofenac sodium (Voltaren).

OBJECTIVE: Although diclofenac sodium (Voltaren) is one of the most frequently prescribed non-steroidal anti-inflammatory drugs (NSAIDs) worldwide for the treatment of inflammation and pain; data on the ultrastructural alterations in renal tissues due to its chronic exposure are limited. Therefore, the present study was designed to identify the ultrastructural renal alterations induced by diclofenac sodium. METHODS: The experiment was conducted at the animal house of the Department of Zoology, College of Science, King Saud University, Riyadh, Kingdom of Saudi Arabia during the period from April 2003 to June 2003. A total of 30 male rabbits were exposed to intraperitoneal injection with a daily dose of diclofenac sodium (1.5 mg/kg body weight) for 70 days to investigate the resultant ultrastructural alterations in renal tissues. RESULTS: In comparison with the respective control rabbits, chronic exposure to therapeutic doses of diclofenac sodium produced significant ultrastructural renal alterations, which involved swelling and cristolysis of the mitochondria, marked dilatation of the endoplasmic reticulum, detachment of ribosomes, increased lysosomal structures, nuclear chromatin condensation in the tubular cells, thickening of the glomerular basement membranes, distention of glomerular capillaries, which showed lodgment of neutrophils, mesangial and endothelial cell proliferation in the glomeruli, swelling and fusion of the glomerular podocytes foot processes with focal obliteration of the filtration slits. CONCLUSION: The obtained results indicate that chronic exposure to diclofenac sodium produces significant ultrastructural alterations in renal tissues.

Histological and histochemical alterations in the kidney induced by lead.

BACKGROUND: Although lead intoxication is one of the most common forms of metal intoxication, the histochemical alterations in the renal tissues due to chronic lead exposure is limited and has not yet been well identified. SUBJECTS AND METHODS: A total of 60 male Wistar albino rats (Rattus norvegicus) were exposed to lead acetate trihydrate (0.0, 0.25, 0.5, 1.0 and 2% for 1 to 12 months) in drinking water to investigate the histological and histochemical alterations in the renal tissues due to lead. RESULTS: Chronic exposure to subtoxic doses of lead produced distinct progressive tubular, glomerular and interstitial damages. Tubular changes occurred earlier than glomerular and interstitial ones, and included anisokaryosis, nuclear pyknosis, karyomeglay, development of intranuclear and cytoplasmic inclusions together with tubular dilation, necrosis, vacuolization, tubular hyperplasia and solid tubular adenoma. The glomerular alterations were mainly mesangial hypercellularity, segmental proliferation, focal and segmental glomeruloscleriosis, glomerural hyalinization and glomerular tuft alterations. CONCLUSIONS: The findings indicate that lead produces significant histological and histochemical changes in the kidney that lead to severe complications.