Determination of nephrotoxicity and genotoxic potential of silver nanoparticles in Swiss albino mice

Silver nanoparticles (AgNPs) possess properties that are important for industrial and medical applications. This study is aimed to investigate intra-peritoneal toxicity of AgNPs at 26, 52 or 78 mg/kg/day for 5 days in mice Swiss albino mice. The effects on oxidative stress markers activities of serum superoxide dismutase (SOD) and catalase (CAT), levels of serum glutathione (GSH), apoptosis (TUNEL assay), DNA strand breaks (comet assay) in lymphocytes, as well as histopathological of kidney tissue were determined. AgNPs significantly increased SOD and CAT activities reduced GSH levels. In kidney apoptosis (TUNEL assay) while DNA strand breaks (comet assay) in lymphocytes revealed that AgNPs at concentration 78 mg/kg produced significant apoptosis and DNA damage. AgNPs also produced associated histological renal tissue damage. Evidence suggests that AgNPs-mediated alterations may be attributed to oxidative stress.     

壬基酚聚氧乙烯醚对斑马鱼精巢组织的影响

采用半静态水体暴露的方式研究了非离子表面活性剂对成熟雄性斑马鱼精巢组织的影响。用荧光定量PCR(qRTPCR)方法检测试验鱼精巢雌激素受体α(ERα)、雄激素受体(AR)基因以及性激素合成相关细胞色素P450酶类基因(CYP17和CYP19a)的表达,通过组织学观察研究受试鱼精巢结构的变化。结果表明,壬基酚聚氧乙烯醚(NPEO)暴露可以引起雄性斑马鱼精巢组织结构的改变,并影响成年雄性斑马鱼ERα、AR基因和性激素合成相关细胞色素P450酶类基因的表达水平,且10.0 mg·L~(-1)的NPEO暴露可以显著上调CYP19a、ERα和AR基因的表达量,可显著下调斑马鱼精巢中CYP17基因的表达量。在组织学上,0.1 mg·L~(-1)组斑马鱼生精小管内不仅生精小囊数目减少,且管腔中精子数量减少,出现非细胞区域; 1.0和10.0 mg·L~(-1)组可见部分个体精子凝聚于生精小管管腔中央,管腔内空隙明显增大,表现出严重的精子浓缩效应。由此表明,NPEO暴露通过抑制CYP17基因的表达干扰睾酮的合成;同时,NPEO暴露通过诱导CYP19a和ER基因的表达增加内源雌激素的合成,导致斑马鱼精巢中性激素紊乱,最终损伤斑马鱼精巢组织。     

Deleterious effects of cypermethrin on rat liver and kidney: Protective role of sesame oil

The involvement of reactive oxygen species (ROS) has been implicated in the toxicity of various pesticides. Our study was designed to investigate the induction of oxidative stress by cypermethrin; a Type II pyrethroid in rat liver and kidney. In addition, the protective role of sesame oil against the toxicity of cypermethrin was investigated. Animals were divided into four equal groups; the first group used as control while groups 2, 3 and 4 were treated with sesame oil (5 mL/kg b.w), cypermethrin (12 mg/kg b.w) and the combination of both sesame oil (5 mL/kg b.w) plus cypermethrin (12 mg/kg b.w), respectively. Rats were daily administered with their respective doses for 30 days by gavage. Repeated oral administration of cypermethrin was found to reduce the level of glutathione (GSH) and the activities of the antioxidant enzymes. While, the level of TBARS was elevated indicating the presence of oxidative stress. The activities of LDH, AST and ALT were decreased in the liver extract while increased in the plasma of the cypermethrin-treated group. Also, the levels of urea and creatinine were significantly increased after treatment with cypermethrin. Liver and kidney injury was confirmed by the histological changes. In conclusion, the administration of sesame oil provided significant protection against cypermethrin-induced oxidative stress, biochemical changes, histopathological damage and genomic DNA fragmentation.     

Neuroprotective potential of N -acetylcysteine in carbofuran neurotoxicity: A biochemical and histopathological study

The present study was undertaken to evaluate biochemical markers of chronic carbofuran exposure to rats in terms of lipid peroxide and intrasynaptosomal calcium levels and to correlate them with the histopathological changes in brain regions. A significant increase in lipid peroxidation (LPO) in terms of thiobarbituric acid reactive substances (TBARS) was observed in the cerebral cortex (65%) and brain stem (33%) after carbofuran exposure. This was accompanied by a significant increase (87%) in the intracellular free-Ca²⁺ [Ca²⁺]_i levels. N-acetylcysteine (NAC) administration, on the other hand, reversed the carbofuran-induced increase in LPO and [Ca²⁺]_i. Histopathological studies of carbofuran-exposed brain revealed high frequency of pyknotic neurons in the cerebral cortex and microhaemorrhages in the brain stem. NAC supplementation to carbofuran-treated animals resulted in normalisation of the brain architecture as seen by a reduction in the number of pyknotic nuclei in the cerebral cortex. These findings indicate that increased LPO and elevated [Ca²⁺]_i levels are involved in the development of carbofuran neurotoxicity and are eventually responsible for the pathological alterations. The study also demonstrates potential neuroprotective effect of NAC treatment in carbofuran neurotoxicity.     

Comparative changes in absorption,distribution and toxicity of copper and cadmium chloride in toads during the hibernation and the role of vitamin C against their toxicity

The aim of this study was to determine the bioavailability and adverse effects of cadmium (Cd) and copper (Cu) on hibernating Egyptian toads and whether ascorbic acid (vitamin C) blocked Cd- and Cu-induced effects during hibernation. The oxidative status of liver, kidney, and intestine of Bufo regularis to Cd, Cu, and/or a combination of both metals administered orally for 2 weeks was determined. In the protection studies, vitamin C was given for 1?h prior to administration of Cu, Cd, and/or metal combination for 2 weeks. Treatment with Cu, Cd, and a combination of both metals produced a reduction in red blood count cells and hemoglobin content, while white blood count cells showed an increase in numbers during these treatments. After 2 weeks exposure, Cd and Cu increased significantly in all the tissues studied. Cu storage presented the following sequence: liver?>?intestine?>?kidney. Cd storage presented the following sequence: intestine?>?kidney?>?liver. When exposed to both metals, Cu and Cd storage presented the following sequence: liver?>?intestine?>?kidney. Histopathological examination of the liver revealed marked alterations including loss of hepatic cell architecture, and some cells exhibited distinct cytoplasmic vacuoles. The majority of blood vessels exhibited a marked dilatation and congestion with infiltration of blood cells, prominent hyperemia of hepatic veins, and significant proliferation of bile ductules. Histopathological changes in the kidney showed destruction and degeneration of both renal tubule cells and glomerular with infiltration of leukocytes and inflammatory cells. Histopathological alterations in the intestine were restricted to the innermost mucosal epithelium with marked degeneration of the villi and submucosa and an extensive fragmentation of mucosal epithelium as well as atrophy of goblet cells. The administration of vitamin C 1?h prior to administration of Cd, Cu, and metal combination did not protect against hepatic, renal, and intestinal damage. However, parental vitamin C given alone increased tissue toxicity.     

Protective role of Curcuma longa extract and curcumin on mercuric chloride-induced nephrotoxicity in rats: evidence by histological architecture

Mercury (Hg) is a potent nephrotoxin. The aim of this study was to investigate the protective role of Curcuma longa extract and curcumin against HgCl₂-induced nephrotoxicity. Male Sprague Dawley rats were administered HgCl₂ (12 μmol kg^?1, ip; once only) followed by treatment of Curcuma longa extract (200 mg kg^?1, po) and curcumin (80 mg kg^?1, po) for three days after 24 h of HgCl₂ administration. The present results showed that mercuric chloride administration caused an impairment of renal function system which was evident from significant increase in urea, creatinine, uric acid, and blood urea nitrogen concentration in serum. In addition, the swelling in glomerulus and degenerated renal tubules with obstructed lumen was also observed by acute mercuric chloride administration. Treatment with Curcuma longa extract and curcumin was effective in restoring all variables of kidney functions near to control group, which was consistent with kidney histoarchitecture. In conclusion, these results suggest that Curcuma longa extract and curcumin protect against HgCl₂-induced nephrotoxicity. This study could be important for the further understanding of mercury toxicity in renal tissues and in the development of better treatments for people and/or animals exposed to the metal.     

Comparative effects of trivalent and hexavalent chromium on spermatogenesis of the mouse

It has been repeatedly stressed that the biological effectiveness of chromium depends entirely on its oxidation state. The present work compares the histological effects of ingested trivalent and hexavalent chromium compounds on the mouse testes. The results showed comparable data of food consumption and gain in body weight. Both compounds produced ambiguous levels of degeneration in the outmost cellular layers of a number of seminiferous tubules, reduced the number of spermatogonia per tubule and the sperm count, and caused significant increases in the percentage of morphologically abnormal sperms. Generally, all these effects were more pronounced in animals which ingested the hexavalent chromium.     

Induction of oxidative stress by benzo(a)pyrene in the epididymis of Wistar rats

The present study was undertaken to evaluate the effect of sub-chronic exposure to benzo(a)pyrene on the antioxidant system and histology of rat epididymal sperm. Intraperitoneal administration of benzo(a)pyrene to male Wistar rats at doses between 1 and 100 µg/kg body weight for 60 days entailed a decrease in the weight of the epididymis (caput and cauda), seminal vesicle, and prostate, while the body weight was not affected. Epididymal sperm reserves were reduced in a dose-dependent manner. Indicators of lipid peroxidation were increased while activities of superoxide dismutase and catalase in all three epididymal regions decreased. Histological malformations were observed in the epididymis. Exposure to benzo(a)pyrene deranges the antioxidant defense system and induces histological changes in the epididymis.     

苯并[a]芘对栉孔扇贝(Chlamys farreri)组织显微和超微结构的影响

在实验条件下研究了苯并[a]芘(B[a]P)暴露对栉孔扇贝的鳃、消化盲囊显微(10d、20d)和超微结构(10d)的影响.观察结果表明,10μg·L-1B[a]P处理10d时,栉孔扇贝的鳃上皮粘液细胞增多,在回血管中血细胞出现聚集现象;消化盲囊腺泡中嗜碱性颗粒增多,腺泡内细胞间界限模糊.超微结构观察可见,鳃上皮纤毛和微绒毛脱落,鳃上皮细胞内次级溶酶体增多,核周池扩大,鳃血腔中出现血细胞坏死后残留的细胞核;在消化盲囊分泌细胞中线粒体嵴减少,出现线粒体缺失形成的空泡,细胞内质网片断化,核糖体脱落.由10μg·L-1B[a]P处理20d时,在鳃回血管中发现血细胞坏死后残留的固缩细胞核,鳃丝的上皮细胞排列不规则甚至断裂,部分消化腺泡崩解,鳃丝结构和消化导管上皮结构损害严重;消化盲囊组织结构的损伤比鳃更为严重.这些组织结构损伤表明,栉孔扇贝在B[a]P胁迫下组织学的变化特征与过程与贝类组织解毒代谢过程相符合.