Renal Cortical Slices: An In Vitro Model for Kidney Metabolism and Toxicity

1992 ◽  
Vol 20 (1) ◽  
pp. 71-76
Author(s):  
Andrea Trevisan ◽  
Stefano Maso ◽  
Paola Meneghetti

The in vitro renal cortical slice model was used to study: 1) the effects on the kidney of some haloalkanes and haloalkenes using 3-month-old male Wistar rats; 2) influence of age and sex on renal cortical slice indices in non-treated rats; and 3) effects of 1,2-dichloropropane on the slices after pretreatment of 3-month-old male Wistar rats with DL-butathionine-[S,R]-sulphoximine. The most nephrotoxic chemical used was 1,3-dichloropropene, which caused a total depletion in the levels of reduced glutathione, a high peroxidation of lipid (about three thousand-fold with respect to control), a significant release of tubular enzymes into the medium, and loss of organic anion ( p-aminohippurate) accumulation. All the chemicals affected the cytosol more than the brush border. The most remarkable age-related differences in the untreated slices were the progressive decrease of reduced glutathione (p<0.05 from three months of age), and an increase in lactate dehydrogenase release into the medium (p<0.05 from six months of age). By contrast, sex differences were slight. The ‘treatment with 1,2-dichloropropane of slices prepared from rats pretreated with DL-butathionine-[S,R]-sulphoximine significantly increased the depletion of glutathione content (p<0.05) and malondialdehyde release in the medium (p<0.001) caused by the solvent alone.

1993 ◽  
Vol 12 (2) ◽  
pp. 117-121 ◽  
Author(s):  
Andrea Trevisan ◽  
Paola Meneghetti ◽  
Stefano Maso ◽  
Ornella Troso

1 Renal cortical slices isolated from the kidneys of male Wistar rats were used as an experimental model for studying the nephrotoxicity induced by 1,2-dichloropropane. 2 The solvent causes a depletion of renal reduced glutathione content and slight, but significant, lipid peroxidation. The block of the oxidative pathway with carbon monoxide prevents glutathione content depletion, and shows that this conjugation is the major step in 1,2-dichloropropane metabolism. 3 Loss of organic anion accumulation and release into the incubation medium of tubular enzymes, mainly from the soluble fraction, are the toxic effects of the solvent. The brush border is only slightly affected. 4 The mechanism of nephrotoxicity appears to occur via mercapturic acid metabolism. Acivicin and aminooxyacetic acid, inhibitors of gammaglutamyltransferase and β-lyase activity, respectively, partially but significantly prevent the loss of organic anion accumulation induced by 1,2-dichloropropane. Furthermore, α-ketobutyrate, an activator of β-lyase, enhances the effects of 1,2-dichloropropane on the target, but is itself toxic for organic anion accumulation.


1999 ◽  
Vol 277 (1) ◽  
pp. H399-H404 ◽  
Author(s):  
Pilar Nava ◽  
Verónica Guarner ◽  
Rosalinda Posadas ◽  
Israel Pérez ◽  
Guadalupe Baños

Insulin-elicited endothelin release in hypertriglyceridemic, hypertensive, hyperinsulinemic (HTG) rats was shown. Weanling male Wistar rats were given 30% sucrose in their drinking water for 20–24 wk. In vitro contractions of aorta and femoral arteries were elicited with 40 mM KCl. Endothelin release induced with KCl plus 50 μU/ml insulin resulted in increases in contractile responses: 41 ± 5.9 and 57 ± 6% for control and 65.5 ± 6 and 95 ± 9% for HTG aortas and femoral arteries, respectively. The endothelin ETB-receptor blocker BQ-788 decreased responses to KCl + insulin by 39 ± 8 and 53 ± 5% in control and 48 ± 13 and 79 ± 3.5% in HTG aortas and femoral arteries, respectively. The ETA-receptor antagonist PD-151242 inhibited these responses by 12 ± 10 and 1 ± 9% in control and by 51.5 ± 9 and 58.5 ± 1% in HTG aortas and femoral arteries, respectively. These results suggest that endothelin may contribute to the hypertension in this model.


2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
R. Francik ◽  
M. Krośniak ◽  
M. Barlik ◽  
A. Kudła ◽  
R. Gryboś ◽  
...  

The aim of this study was to investigate the clinical efficacy of vanadium complexes on triglycerides (TG), total cholesterol (Chol), uric acid (UA), urea (U), and antioxidant parameters: nonenzymatic (FRAP—ferric reducing ability of plasma, and reduced glutathione—GSH) and enzymatic (glutathione peroxidase—GPx, catalase—CAT, and GPx/CAT ratio) activity in the plasma of healthy male Wistar rats. Three vanadium complexes: [VO(bpy)2]SO4⋅2H2O, [VO(4,4′Me2bpy)2]SO4⋅2H2O, and Na[VO(O2)2(bpy)]⋅8H2O are administered by gavage during 5 weeks in two different diets such as control (C) and high fatty (F) diets. Changes of biochemical and antioxidants parameters are measured in plasma. All three vanadium complexes statistically decrease the body mass growth in comparison to the control and fatty diet. In plasma GSH was statistically increased in all vanadium complexes-treated rats from control and fatty group in comparison to only control group. Calculated GPX/CAT ratio was the highest in the control group in comparison to others.


2014 ◽  
Vol 66 (3) ◽  
pp. 1075-1081
Author(s):  
Ivan Simic ◽  
Violeta Iric-Cupic ◽  
Rada Vucic ◽  
Marina Petrovic ◽  
Violeta Mladenovic ◽  
...  

The aim of the present study was to evaluate the subchronic effects of 3,4-methylenedioxymethamphetamine on several oxidative stress markers: index of lipid peroxidation (ILP), superoxide dismutase (SOD) activity, superoxide radical (O2.-) levels, and reduced glutathione (GSH) levels in the frontal cortex, striatum and hippocampus of the rat. The study included 64 male Wistar rats (200-250g). The animals were treated per os with of 5, 10, or 20 mg/kg of 3,4-methylenedioxymethamphetamine (MDMA) every day for 15 days. The subchronic administration of MDMA resulted in an increase in ILP, SOD and O2.-, and a decrease in GSH, from which we conclude that oxidative stress was induced in rat brain.


2020 ◽  
Vol 1 (1) ◽  
Author(s):  
Ester G Panserga ◽  
Cecep S Kristanto ◽  
Budi Pratiti ◽  
Patricia Wulandari

Abstract Introduction Antipsychotics are drugs that are widely prescribed for mental disorders, such as schizophrenia and psychosis. Recent in vitro studies show antipsychotics play a role in the initiation of neuronal cell apoptosis. This study aims to determine the effect of haloperidol and risperidone on neuronal cell apoptosis in Wistar white rats. Methods Male wistar rats aged 8 weeks (n = 30) were used in this study. Wistar rats were randomized into 6 groups. Group A: 5 wistar rats as a control without induced schizophrenia, aquades and drugs. Group B: 5 Wistar-induced psychotic mice (using 30 mg / kgBB ketamine, intraperitoneal injection for 5 days) and aquadest. Group C: 5 rats were induced psychotic and were given haloperidol or 0.05 mg / kgBB orally, for 28 days. Group D: 5 mice were induced psychotic and were given haloperidol 0.1 mg / kg orally, for 28 days. Group E: 5 mice were induced psychotic and were given risperidone 0.05 mg / kgBB orally, for 28 days. Group F: 5 mice were induced psychotic and given risperidone 0.1 mg / kgBB orally, for 28 days. Apoptosis of neuronal cells in the ventral tegmental area was assessed by caspase-3 immunohistochemistry. The colored area will be calculated as a total percentage using the imageJ program. Results Risperidone and haloperidol increase caspase-3 activity, but haloperidol increases caspase-3 activity more than risperidone. Conclussion Risperidone and haloperidol induce apoptosis of neuronal cells and tardive dyskinesia in Wistar rats with psychotic models.


PLoS ONE ◽  
2020 ◽  
Vol 15 (7) ◽  
pp. e0236298
Author(s):  
Lindsay J. Bailey-Steinitz ◽  
Ying-Hsuan Shih ◽  
Monte J. Radeke ◽  
Pete J. Coffey

2019 ◽  
Vol 87 (3) ◽  
pp. 24 ◽  
Author(s):  
Emeka Eze Joshua Iweala ◽  
Winifred Osa Evbakhavbokun ◽  
Emmanuel Ndubisi Maduagwu

N-Nitrosodiethylamine (NDEA) is a nitrosamine derivative with carcinogenic and mutagenic properties which can be found in tobacco smoke, meat and various food products. This study examined the antioxidant and hepatoprotective potential of Cajanus cajan (C. cajan) with respect to hepatotoxicity in male Wistar rats. Administration of NDEA induced hepatotoxicity at 200 mg/kg while C. cajan was administered (200, 400 and 800 mg/kg) for 28 days. NDEA-induced hepatotoxicity significantly (p ≤ 0.05) increased alanine aminotransferase (ALT), aspartate aminotransferase (AST) and malondialdehyde (MDA) and significantly (p ≤ 0.05) decreased reduced glutathione (GSH), albumin (ALB), glutathione S-transferase (GST), catalase (CAT) and superoxide dismutase (SOD). C. cajan-treated groups were seen to have significantly (p ≤ 0.05) decreased ALT and AST and significantly (p < 0.05) increased ALB, GST, GSH, SOD and CAT. The NDEA-treated group also showed a marginal increase in body weight and a significant (p ≤ 0.05) increase in liver weight. The C. cajan treated groups showed a significant (p ≤ 0.05) increase and decrease respectively in body and liver weights. Histopathological changes also substantiated NDEA-induced hepatotoxicity and the hepatoprotective effect of C. cajan on the liver. The results indicate that C. cajan has the potential to ameliorate NDEA-induced hepatotoxicity.


2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Silvia Bona ◽  
Lidiane Isabel Filippin ◽  
Fábio Cangeri Di Naso ◽  
Cintia de David ◽  
Bruna Valiatti ◽  
...  

Aim. This study aimed to assess the antioxidant activity of quercetin (Q) in an experimental model of cirrhosis induced by CCl4 inhalation. Materials and Methods. We used 25 male Wistar rats (250 g) that were divided into 3 groups: control (CO), CCl4, and CCl4+Q. The rats were subjected to CCl4 inhalation (2x/week) for 16 weeks, and they received phenobarbital in their drinking water at a dose of 0.3 g/dL as a P450 enzyme inducer. Q (50 mg/Kg) was initiated intraperitoneally at 10 weeks of inhalation and lasted until the end of the experiment. Statistical analysis was by ANOVA Student Newman-Keuls (mean±SEM), and differences were considered statistically significant when P<0.05. Results. After treatment with quercetin, we observed an improvement in liver complications, decreased fibrosis, as analyzed by picrosirius for the quantification of collagen, and decreased levels of matrix metalloproteinase 2 (MMP-2) compared with the CCl4 group. It also reduced oxidative stress, as confirmed by the decrease of substances reacting to thiobarbituric acid (TBARS), the increased activity of antioxidant enzymes, and the reduced glutathione ratio and glutathione disulfide (GSH/GSSG). Conclusion. We suggest that the use of quercetin might be promising as an antioxidant therapy in liver fibrosis.


2003 ◽  
Vol 90 (3) ◽  
pp. 565-571 ◽  
Author(s):  
Megumi Nishimukai ◽  
Hiroshi Hara ◽  
Yoritaka Aoyama

As the physiological roles of dietary lecithin have not yet been clearly defined, we examined the effects of lecithin on lipid absorption in male Wistar rats with a mesenteric lymph cannula. Lymphatic absorption was observed after the infusion of 1 ml emulsion containing 100 mg test oil emulsified with sodium taurocholate (10 g/l) in three separate experiments. Test oils (100 mg) were: soyabean oil (triacylglycerol (TG) source, SO) and soyabean oil + lecithin (75 mg soyabean oil+25 mg lecithin, LE) in Expt 1; SO, LE or soyabean oil + lysolecithin (75 mg soyabean oil plus 25 mg lysolecithin, LY) in Expt 2; hydrolysed soyabean oil (HSO) or HSO+lysolecithin (75 mg HSO+25 mg lysolecithin, HLY) in Expt 3. After LE and LY infusions, lymph flow and the lymphatic output of TG was higher than after SO infusion at 0-30 min and 0-90 min respectively (Expts 1 and 2). Lecithin-induced increases in lymph TG output remained constant when HSO was infused (Expt 3). There were no differences in the TG:phospholipid ratio in the lymph after infusion among the groups; nevertheless, the lymphatic output of TG was much higher after infusion with LE than with SO. Fatty acid was released more efficiently from SO than from LE and LY by in vitro digestion with rat bile–pancreatic juice. These present results demonstrate that a TG emulsion containing soyabean lecithin or its hydrolysates promote lymphatic TG output and suggest that the increases in TG absorption do not depend on TG digestion.


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