Organ Histopathological Changes and its Function Damage in Mice Following Long-term Exposure to Lanthanides Chloride

Due to increasing applications of lanthanides (Ln) in industry and daily life, numerous studies confirmed that Ln exposure may result in organ damages in mice and rats, while very few studies focused on several organs damages simultaneously. In order to compare the toxicity of Ln on organs, mice were exposed to LaCl(3), CeCl(3), and NdCl(3) of a dose of 20 mg/kg body weight for consecutive 60 days, respectively, then histopathological changes of liver, kidney, and heart, and their function were investigated. The results showed that long-term exposure to Ln caused cell necrosis and basophilia of liver, ambiguity of renal tubule architecture, congestion of blood vessel and capillary of kidney, and heart hemorrhage. The histopathological changes of liver, kidney, and heart in mice caused by Ce(3+) was most severe; the effect by Nd(3+) was slighter than Ce(3+) but more severe than La(3+). The assay of serum biochemical parameters suggested that Ln exposure severely impaired the functions of liver, kidney, and myocardium in mice. These findings suggested that long-term exposure to Ln resulted in histopathological changes of liver, kidney, and heart, and their function damages. Therefore, we thought that long-term application of the products containing Ln on human should be cautious.     

Protective effects of selenium against mercury toxicity as studied in the rat liver and kidney by nuclear analytical techniques

Mercuric chloride and sodium selenite were separately administered to male rats in the drinking water or in a combination (2.5 mmol Hg/L and 0.1 mmol Se/L). The mercuric chloride group showed histopathological lesions, as evidenced by cell necrosis in the liver and tubular necrosis in the kidney. The sodium selenite group showed some depression in growth, but pathological changes were found neither in the liver nor in the kidney. Simultaneous administration of both compounds produced a protective effect on weight loss and histopathology. These effects were associated with some small structures in the kidney proximal tubules and to some structure in the extracellular space in the liver. Thin, unstained cryosections were freeze-dried and examined in the Studsvik Nuclear Microprobe. The structures observed in the liver and the kidney were shown to contain both selenium and mercury.     

Shilajit potentiates the effect of chemotherapeutic drugs and mitigates metastasis induced liver and kidney damages in osteosarcoma rats

Osteosarcoma is a primary malignant cancer of the bone identified by the direct formation of osteoid tissue or immature bone by cancer cells. The liver and kidneys represent two major secondary organs to which osteosarcoma metastasizes. In this study, we assessed Shilajit, a phytomineral diffusion traditionally used in Ayurvedic medicine, for its possible protective effects against metastasis induced liver and kidney damages in an osteosarcoma rat model. Osteosarcoma rats displayed typical dysregulation of serum levels of hepatic and renal functional markers (p < 0.05) including aspartate aminotransferase (AST)* and alanine aminotransferase (ALT), alkaline phosphatase (ALP), total proteins, albumin, bilirubin, creatinine, urea, and uric acid. Changes in functional markers were also positively correlated with marked histopathological alterations in liver and kidney tissues. Whereas Shilajit's treatment of osteosarcoma rates in combination with CMF (cyclophosphamide, methotrexate, and 5-fluorouracil) chemotherapy drug cocktail significantly (p < 0.05) reversed the studied functional markers to their near-normal levels. Co-treatment of shilajit and drug cocktails also markedly alleviated histopathological changes in liver and kidney tissues. Correlation co-efficient analysis of hepatic and renal functional markers revealed a significant inter-association among these markers. Collectively, present data indicate that shilajit may potentiate the effects of chemotherapy drugs and mitigate the metastasis-induced liver and kidney damage in osteosarcoma. Thus, the findings of this study substantiate the beneficial health effects of shilajit and promote its regular consumption.     

Histopathological Changes of Hepatorenal Toxicity Induced by Gentamicin in Killifish,Aphanius hormuzensis (Aphaniidae) and its Kidney Regeneration Through Nephron Neogenesis

Journal of Ichthyology - The histopathological changes in liver and kidney toxicity after induction by gentamicin are studied in killifish, Aphanius hormuzensis, and its kidney regeneration through...     

Uranium distribution in broiler organs and possibilities for protection

The aim of the present study was to investigate the distribution of uranium (uranyl nitrate hexahydrate, UN) in muscle and organs (kidney, liver, and brain) of broilers, after a 7-day contamination with UN and administration of two different adsorbents (organobentonite and organozeolite). The birds were contaminated during 7 days with 25 mg/UN per day. Adsorbents were given via gastric tube, immediately after contamination with UN. In group 1 that did not receive any adsorbents, histopathological changes in the contaminated broilers were observed in small intestine, liver, and kidney in the form of necrosis of intestinal villi, oedema and cytoplasmic vacuolation of hepatocytes, and dystrophic changes in the kidney tubules epithelium. Organobentonite administered via gastric tube (group 2) reduced uranium distribution by 66 % in kidney, 81 % in liver, and 34 % in brain. In group 3, administration of organozeolite reduced uranium distribution by 67 % in kidney, 68 % in liver, and 49 % in brain. In groups 2 and 3, where the broilers received adsorbents immediately after the UN contamination, no histopathological lesions were observed.     

Arteriosclerosis in the influx and intravisceral arteries of the liver, kidney and lung of WHHL rabbits.

We performed a histopathological investigation on arteriosclerotic development in the influx and intravisceral arteries of the liver, kidney and lung of male WHHL rabbits. In the influx arteries of these organs, we observed severe atherosclerotic vascular lesions with high-grade luminal stenosis. In the intravisceral arteries of the liver and kidney, no arteriosclerotic lesions were observed. However, in the intrapulmonary arteries, we recognized severe atherosclerotic vascular changes with high-grade stenosis or total obstruction of the lumen in some middle to large sized pulmonary arteries. These observations indicate that the development of arteriosclerosis in parenchymatous organs differs, and that some organs are predisposed to arteriosclerosis formation.     

Chronic effects of cadmium on kidney,liver, testis,and fertility of male rats

Male Wistar rats (n:20), at 5 wk of age, were given cadmium in drinking water (10 mg/L water) for 52 wk; 8 males and 20 female rats, as controls, were given tap water. At the end of 28 and 40 wk, some of the cadmium-treated males and control group male rats were sacrificed for the histopathological examination of testis, kidney, and liver. At the end of 56 wk, histopathological examinations were performed in the same way. Liver, kidney, and testis cadmium levels were also determined by atomic absorption spectrophotometry. All the cadmium-treated male rats showed pathological testicular alterations, and liver and kidney damage after chronic exposure. Cadmium levels were found to be highest in the kidney (1.009 +/- 0.034 microgram/g wet tissue in the infertile group). At the end of the 52-wk period, reproductive capacity of the cadmium-treated rats was investigated and was found to be lost in 39.89% of the animals.     

Bradykinin potentiating factor isolated from Buthus occitanus venom has a protective effect against cadmium-induced rat liver and kidney damage

Bradykinin and its related peptides are widely distributed in venomous animals, including scorpion. A peptide fraction isolated from the venom of the Egyptian scorpion Buthus occitanus was proved to have a bradykinin-potentiating activity. The aim of the present study was conducted to investigate whether the treatment with bradykinin potentiating factor (BPF) offers more beneficial effects in reversing cadmium-induced oxidative stress in rat liver and kidney. Adult male rats, equally divided into control and two treated groups, 10 animals in each group. group (I) was orally given (1 ml) saline and served as a control group; group (II) of rats was given cadmium chloride (4 mg/kg) alone, once daily an oral dose for 7 successive days; group (III) of rats was given ip injection (1 ml) BPF, once daily a dose for 7 successive days prior to CdCl₂ treatment and on the next 7 successive days with the same dose of cadmium as group II. Both organs were subjected to histopathological analysis with the light microscope. The activities of alanine aminotransferase (ALT), asparate aminotransferase (AST) and alkaline phosphatase (ALP) in serum were measured as indicators of the liver function. As parameters of the kidney function, creatinine, uric acid and urea concentrations in serum were determined. Also, malondialdehyde (MDA), reduced glutathione (GSH), super oxide dismutase (SOD) and catalase (CAT) were determined in both tissues. Cd exposure caused a significant decrease or inhibition in the activities of GSH, SOD, and CAT, with significant increase in the level of MDA, in versus to control groups in both liver and kidney. Also, when Cd was treated in co-administration with BPF induced increase or stimulation in the activity of GSH, SOD, and CAT, with significant decrease in the level of MDA when compared to Cd group in both organs. Histopathological changes of liver and kidney were also in accordance with the biochemical findings. Our data showed that Cd treatment induced histopathological alteration in the liver, severe hydropic degeneration in centrolobular zones. Inflammatory cells infiltration around the congested central vein and an obvious injury in some renal tubules. Bradykinin potentiating factor (BPF) administration prevented the histopathological alterations which observed in Cd-groups and both liver and kidney had essentially normal appearance in histopathological examination. In conclusion, BPF markedly ameliorated cadmium-induced liver and kidney tissue damage as evidenced by histological and biochemical examinations and acts as a potent scavenger of free radicals to protect the liver and kidney against the deleterious effect of acute cadmium intoxication.     

Oxidative stress parameters in blood, liver, and kidney of diabetic rats treated with curcumin and/or insulin

This study evaluated the effects of curcumin and/or insulin on antioxidant enzyme activity in blood, liver, and kidney, as well as on lipid peroxidation and delta aminolevulinic dehydratase (δ-ALA-D) activity, and a histopathological analysis of streptozotocin-induced diabetic rats. The animals were divided into six groups (n = 6): control/saline (C); control/curcumin (CCur); diabetic/saline (D); diabetic/insulin (DIns); diabetic/curcumin (DCur); and diabetic/insulin/curcumin (DInsCur). After 30 days of treatment with curcumin and/or insulin, the animals were sacrificed and the liver, kidney, and serum were used for experimental determinations. Results of histopathological analysis showed that the treatment with insulin ameliorate renal and hepatic lesions from both DIns and DInsCur groups. TBARS levels were significantly increased in serum, liver, and kidney in D group and the administration of curcumin and insulin prevented this increase in DIns and DCur groups. The activities of catalase (CAT), superoxide dismutase, and δ-ALA-D presented a significant decrease in the liver and kidney D group when compared to C group (P < 0.05). The animals treated with curcumin and insulin presented an increase of CAT activity, revealing a positive interaction between both substances. The treatments with curcumin or insulin prevented oxidative stress in blood, through modulation of enzymatic antioxidant defenses. These findings contributed to the comprehension that antioxidants from medicinal plants could be used as adjuvant in the treatment of this endocrinopathy and not as single therapy.     

Carbendazim generates symplasts in rat spermatogenic clones.

In order to find non-microtubular targets in the seminiferous epithelium for the fungicide and reproductive toxicant carbendazim, it was administered to 90 days old male Wistar rat in a single bolus dose of 400 mg/kg body weight through an oral intubation. A parallel control group was maintained. Rats were sacrificed 48 days after the treatment and the testes were analysed for histopathological changes adopting routine histological methods, when symplasts were localised. The maximum diameter of five largest symplasts was measured, and the number of nuclei in these symplasts was also determined. As it is known that symplasts of spermatogenic cells are produced due to opening up of the intercellular bridges between cells in a clone consequent upon disruption of actin microfilaments, the present study shows that actin microfilaments would also be targets in the seminiferous epithelium for carbendazim toxicity.     

Fatal case of salmonellosis (Salmonella pullorum) in a chimpanzee (Pan troglodytes) in the Jos Zoo

A case of salmonellosis in a captive chimpanzee (Pan troglydytes) is reported. Confirmatory diagnosis was based on clinical signs, necropsy and histopathological examination, and the isolation of Salmonella pullorum from the lung, liver, kidney and intestines of the animal. The source of infection was not ascertained.     

花色苷提取物对大鼠发育关键期铅致肝脏和肾脏损伤的保护作用研究

为研究天然色素花色苷（anthocyanins,ACNs）对铅中毒引起的脏器损伤的保护作用,构建了铅暴露大鼠模型,灌服不同剂量的ACNs溶液和强力排铅药二巯基丁二酸（dithioglysuccinic acid, DMSA）,连续3周,于末次给药24 h后考察脏器中的铅含量、组织病理学、血液及脏器生化指标;并采用综合生物标志物响应（integrated biomarker responses, IBR）评估ACNs对铅致发育期大鼠肝脏和肾脏氧化损伤的修复能力。实验结果表明,铅大量存在于大鼠的肝脏和肾脏组织中,造成脏器病理学结构及氧化损伤;而ACNs可促进铅排出机体,改善组织病理学结构,使血清中转氨酶、肌酐等生化指标水平明显好转,并升高肝和肾抗氧化酶的活性,减少还原性物质的含量,改善铅诱导组织的氧化损伤;IBR分析结果显示,ACNs可使铅损伤的脏器得到明显的修复。结果表明,ACNs营养干预可有效拮抗铅致机体的氧化损伤,从而有效修复铅损伤的肝肾组织。     

A prolonged hematopoietic disturbance associated with aortic aneurism and splenomegaly in a squirrel monkey (Saimiri sciureus). A case report.

In a squirrel monkey (Saimiri sciureus), monitored clinically for five years, histopathological review revealed diffuse lymphoblastic lymphocytes infiltrating the thyroid, kidney, liver, pancreas, adrenal medulla, internal fat, extramedullary hematopoietic foci in the spleen and liver, and a mild chronic peritonitis.     

爱德华氏菌人工经口感染及病理观察

用从病鱼体内分离到的福建爱德华氏茵（Ｅｄａｗａｒｄｓｉｅｌｌａｆｕｊｉａｍｅｎｓｉｓ）人工经口感染鳗鲡获得成功,证明该菌由消化道传染。人工感染后一系列组织病理观察表明：该菌对肝脏的损害是致肝细胞融解形成灶性坏死,对肾脏引起造血组织增生。当继发感染气单胞菌（Ａｅｒｏｍｏ－ｎａｓ）后,灶性坏死区形成脓肿。继发感染是爱德华氏病致死的原因,同时也是鳗鲡爱德华氏病症伏表现为肝脏型或肾脏型两种类型的原因。     

Modulation of acute cadmium toxicity by Emblica officinalis fruit in rat

The efficacy of Emblica officinalis in modifying the acute cytotoxicity of cadmium in male rats was evaluated. Oral administration of Emblica fruit juice (500 mg/kg, b.w.) for 8 days followed by a single toxic dose of Cd as CdCl2 (3 mg/kg,b.w. ip), considerably reduced the mortality in rats as well as prevented to some extent the cadmium induced histopathological damage in testis, liver and kidneys. Biochemical investigation also revealed reduced levels of Cd induced serum glutamate oxaloacetate transaminase, glutamate pyruvate transaminase and gamma glutamyltranspeptidase. The enhanced levels of Cd and lipid peroxidation in liver, kidney, and testes and metallothionein and total sulphydryl in liver and kidney by Cd were significantly reduced by Emblica pretreatment. These results suggest cytoprotective potential of Emblica fruit in acute cadmium toxicity which could be due to its multiple role in biological system.     

Evaluation of Two Monitoring Approaches to Assess Effects of Waste Water Disposal on Histological Alterations in Fish

An active monitoring (caging experiment) and a passive monitoring (sampling of wild fish) were performed to investigate the effects of effluent from a sewage treatment works (STW) on brown trout (Salmo trutta) by histopathological examinations of the skin, gill, liver and kidney. Histopathological lesions were evaluated according to a standardised assessment tool, which allows calculation of indices for every organ. According to the results of both monitorings, trout exposed to river water supplemented with treated waste water from the STW Lyss showed higher histopathological indices than trout caught upstream of the discharge point of the STW or kept in river water only. These results indicate a negative effect of treated waste water from the STW on the histopathological status of the examined organs of brown trout. Both monitoring approaches revealed the liver to be the most affected organ compared with reference fish. However, data from the two monitoring approaches were not completely consistent: histologically the gills were the most sensitive organ to the effects of treated waste water in the active monitoring, but were not affected in the passive monitoring. The data provide relevant information about both the comparability and the pros and cons of the two monitoring approaches to assess effects of pollution on histopathological alterations in fish.     

Protective effects of fennel oil extract against sodium valproate-induced hepatorenal damage in albino rats

Foeniculum vulgare (Apiaceae) is commonly known as fennel. This herb is well-known worldwide and traditionally used as curative herbal therapy for the treatment of epileptic disease, seizurescarminative, digestive, lactogogue, diuretic, treating respiratory and gastrointestinal disorders. The aim of present study is to investigate the possible effect of fennel oil against the toxicity of Sodium-Valproic (SVP) in albino rats. In order to assess the protection of fennel oil on SVP induced hepato- and nephro-toxicity, male albino rats were treated with 1 ml/kg b.w fennel oil 3 days/week for 6 weeks. The biochemical analyses of hepatic enzymes were evaluated by estimating blood biomarkers of liver and renal damage along with histological examination. The results obtained from this work showed that treating animals with SVP lead to many histopathological alterations in the liver and kidney tissues. The effect appeared in the liver tissue include leukocyte infiltrations, cytoplasmic vacuolization of the hepatocytes, fatty degeneration and congestion of blood vessels. This commonly used chemical (SVP) caused some unwanted effects on the kidney cortex which histologically observed as degeneration in renal tubules, atrophy of the glomeruli and edema. Biochemical results also revealed an abnormal increase in the enzyme level of AST, SAT, ALP, bilirubin, creatinine and urea-nitrogen, with a noticed decrease in total protein content. However, the results of treated rats with SVP plus fennel oil showed some positive histopathological changes in both the liver and kidney tissues. These results have confirmed that fennel oil has positive effects on the histological structure of the liver and kidney and the biochemical levels of AST, ALT, ALP, bilirubin, total proteins, creatinine and urea. It is concluded that fennel oil has various pharmacological properties including antioxidant, anti-cancer activity, anti-inflammatory. These valuable effects might be due to the presence of aromatic compounds trans-anethole. This useful properties of fennel plant could be due to its antioxidant activity that prevents the toxicity of SVP.     

Apigenin protects from hepatorenal damage caused by lead acetate in rats

Exposure to lead (Pb) is associated with serious health problems including hepatorenal toxicity. Apigenin is a natural-sourced flavonoid with promising antioxidant and anti-inflammatory effects. In this research, we investigated the potential protective role of apigenin against lead acetate (PbAc)-induced hepatorenal damage. Thus, this experiment studied the exposure of male Wistar Albino rats to apigenin and/or PbAc and their effects in comparison to the control rats. Apigenin administration decreased the levels of Pb and prevented the histopathological deformations in liver and kidney tissues following PbAc exposure. This was confirmed by the normalized levels of liver and kidney function markers. Additionally, apigenin inhibited significantly oxidative reactions through upregulating Nrf2 and HO-1, and activating their downstreamed antioxidants accompanied by a marked depletion of pro-oxidants. Moreover, apigenin decreased the elevated pro-inflammatory cytokines and inhibited cell loss in liver and kidney tissues in response to PbAc intoxication in both tissues. The obtained results demonstrated that apigenin could be used to attenuate the molecular, biochemical, and histological alterations associated with Pb exposure due to its potent antioxidant, anti-inflammatory, and antiapoptotic effects.