Kidney Function In Rats Research Articles

Wheat germ and vitamin E decrease BAX/BCL-2 ratio in rat kidney treated with gentamicin

The intracellular accumulation of gentamicin acts on mitochondria directly (by increasing oxidative stress) and indirectly (by increasing the proapoptotic BAX gene expression levels) and thus activates intrinsic pathway of apoptosis. This study intended to investigate the probable prophylactic effect of wheat germ as a nephro-protective agent in relation to vitamin E as a well-known natural antioxidant on a nephrotoxic model induced by gentamicin. Forty male Sprague Dawley rats were divided randomly into four groups; of 10 rats each: control group, gentamicin group (120 mg/kg/day i.p. for 15 days), vitamin E group (200 mg/kg orally for 45 days) and wheat germ group (20% of the diet for 45 days). Gentamicin injection was started on the 30th day for both groups (3) and (4). It was noticed that wheat germ significantly decreased BAX/BCL-2 ratio. The significant decrement in MDA level and the significant increment in total antioxidant capacity (TAC) level and catalase (CAT) activity of wheat germ treated rats reflecting its antioxidant activity. Additionally, the wheat germ succeeded in improvement of the kidney function of rats of this group which was manifested by amelioration of deteriorated serum creatinine, urea, sodium and potassium levels. In conclusion, the efficacy of wheat germ as anti-apoptotic and antioxidant was higher than that of vitamin E and it effectively protected against the direct and indirect toxic effects of gentamicin on kidney through regulation of BAX-BCL-2 gene expressions and further inhibition of mitochondrial cytochrome c translocation into cytosol.

Effect of sea cucumbers Holothuria atra extract on liver and kidney functions in rats

Sea cucumbers are an abundant group of motile reef invertebrates. They have a special organ called Cuvierian organ that contains toxic substances. The present study aims to show the effect of the sublethal dose of the extract of sea cucumber Holathuria arta on liver and kidney functions in rats at different intervals (half hour, one hour, 6 hours, 12 hours and 24 hours). Specimens of sea cucumbers were collected from the Red sea, Egypt. The sublethal dose (LD25) of the extract of sea cucumber Holothuria atra showed that GOT/AST was not significantly affected although serum GPT/ALT (normal serum level 70.8±3.25 g/ L) was significantly increased reaching maximum value after 6 hours of injection (90.3%) then decreased throughout the experiment. Serum albumin wasn’t significantly affected after injection with (LD25). Also, the total protein didn’t show significant change. The kidney function of the rat was measured by urea and creatinine after injection of (LD25) of the extract of sea cucumber Holothuria atra. Urealevel showeda sharp significant increase and reaching its maximum value after 6 hours of injection (122%), then decreased throughout the experimental period and became non significantly effective after 12 hours. On the other hand, creatinine also showed a significant increase reaching maximum value after 6 hours of injection (112.5%) then decreased through the experiment as urea but it reached normal level after 24 hours. In conclusion, the extract toxin of sea cucumber of Holothuria atra has direct effect on ALT with no other effect on liver function test parameters, while it has sharp effect on kidney function test parameters.

The influence of oxazaphosphorine agents on kidney function in rats

Background and objectiveThe application of cytostatic oxazaphosphorines such as cyclophosphamide (CP) and ifosfamide (IF) is associated with the risk of kidney damage that, depending on the type of drug, dose and route of administration, adopts a different clinical entity and severity. The aim of our study was to assess the influence of CP and IF on the kidney histology and function in rats intraperitoneally treated with four doses of either CP or IF. Materials and methodsA total of 30 rats were divided into three groups (10 in each group): group 1 (control), sham treated with saline solution, group 2 (treated with 75mg/kg b.w. of CP), and group 3 (treated with 60mg/kg b.w. of IF). After the treatment rats were sacrificed, blood was collected and nephrectomy and cystectomy were performed. Qualitative and quantitative parameters (including neutrophil gelatinase-associated lipocalin-1, NGAL-1) of kidney function were assayed in urine and plasma. ResultsCP-treated rats were characterized by a significant polyuria, decreased urine pH and by decreased daily urinary excretion of sodium, potassium, urea and uric acid accompanied by increased NGAL-1 excretion. A significant decrease of the plasma uric acid concentration was also observed. IF-treated animals were also characterized by decreased urine pH but with normal daily urinary excretion of assessed substances (except for reduced uric acid excretion).Both CP and IF treated rats did not show any histopathological abnormalities in their kidneys. ConclusionsCP caused more advanced kidney dysfunction and some indices suggested the development of prerenal acute kidney injury. In the CP-treated group some particularly marked urinary and plasma uric acid disturbances suggested compensation of increased oxidative stress as uric acid is considered to exert also antioxidant properties.

Biochemical and Histological Evaluation of Kidney Function in Rats after a Single Administration of Cyclophosphamide and Ifosfamide

Biochemical and Histological Evaluation of Kidney Function in Rats after a Single Administration of Cyclophosphamide and Ifosfamide

Evaluation of Bacillus subtilis SPB1 biosurfactant effects on hyperglycemia, angiotensin I-converting enzyme (ACE) activity and kidney function in rats fed on high-fat–high-fructose diet

This study investigated the protective and the curative effects of Bacillus subtilis SPB1 crude lipopeptide biosurfactant in alleviating induced obesity complications in rats fed on high-fat–high-fructose diet (HFFD). Male Wistar rats were divided into five groups with the following treatment schedule: normal diet-fed rats (CD), HFFD-fed rats, HFFD-fed rats supplemented with SPB1 biosurfactant from the first day of the experiment (HFFD + Bios1), rats fed on HFFD receiving standard drug (HFFD + Torva), or SPB1 biosurfactant (HFFD + Bios2) during the last 4 weeks of the study. HFFD induced hyperglycemia, manifested by a significant (p < 0.001) increase (20%) in the levels of glucose and α-amylase activity in the plasma, when compared with CD. The administration of SPB1 biosurfactant to rats fed on HFFD reverted back normal blood glucose and α-amylase activity levels. Also, the findings clearly showed that acute oral administration of SPB1 biosurfactant reduced significantly (34%) the peak of blood glucose concentration 60 min after glucose administration, as compared with untreated rats fed on HFFD. Furthermore, renal dysfunction indices such as creatinine and urea as well as the level of angiotensin I-converting enzyme (ACE) exhibited remarkable increases in serum of rats fed on HFFD by 28.35%, 46%, and 92%,. Interestingly, SPB1 lipopeptides treatments decreased the creatinine and urea levels significantly (p < 0.001) near normal values, as compared with that of the HFFD group, and also showed an improvement of the kidney cortex architecture. Moreover, SPB1 biosurfactant displayed a potent inhibition of ACE activity in vitro (CI50 value= 1.37 mg/mL) as well as in vivo in obese rats by 42% and 27.25% with HFFD + Bios1 and HFFD + Bios2 treatments, respectively, and comparatively with the HFFD group. Besides, SPB1 lipopeptides treatments improved some of serum electrolytes such as Na+, K+, Ca2+ , and Mg2+. The results showed that SPB1 lipopeptide biosurfactant presented useful hypoglycemic and antihypertensive properties, and was able to alleviate renal lipid deposition in rats fed on a hypercaloric diet.

English

This study determined the therapeutic effect of ethanol leaf extract of Combretum zenkeri on kidney function of rats exposed to benzo[a]pyrene. Male Wistar albino rats were&nbsp; treated with ethanol leaf extract of C. zenkeri (400 mg/kg) in the presence or absence of BaP (200 mg/kg) for four weeks. The blood obtained at the end of the treatment was processed into serum and used for biochemical analyses and kidney tissues for histology. The serum creatinine, urea, sodium ion and potassium ion concentrations of the group exposed to benzo[a]pyrene without treatment with C. zenkeri extracts were significantly higher (p&lt;0.05) as compared to the normal control group. The kidney histology indicated severely damaged glomeruli. The groups treated with the leaf extract pre- or post- benzo[a]pyrene exposure showed significant reduction (p&lt;0.05) in serum concentration of urea, creatinine and sodium ion, while the pre-treated group showed no significant reduction (p&lt;0.05) in serum potassium ion concentration. The biochemical and histological studies indicated that, C. zenkeri can ameliorate benzo[a]pyrene induced oxidative kidney damage. Key words: Combretum zenkeri, benzo[a]pyrene, PAHs, oxidative damage, kidney functions.

Modulation of renal oxygenation and perfusion in rat kidney monitored by quantitative diffusion and blood oxygen level dependent magnetic resonance imaging on a clinical 1.5T platform.

BackgroundTo investigate the combined use of intravoxel incoherent motion (IVIM) diffusion-weighted (DW) and blood oxygen level dependent (BOLD) magnetic resonance imaging (MRI) to assess rat renal function using a 1.5T clinical platform.MethodsMultiple b-value DW and BOLD MR images were acquired from adult rats using a parallel clinical coil arrangement, enabling quantitation of the apparent diffusion coefficient (ADC), IVIM-derived diffusion coefficient (D), pseudodiffusion coefficient (D*) and perfusion fraction (f), and the transverse relaxation time T2*, for whole kidney, renal cortex, and medulla. Following the acquisition of two baseline datasets to assess measurement repeatability, images were acquired following i.v. administration of hydralazine, furosemide, or angiotensin II for up to 40 min.ResultsExcellent repeatability (CoV <10 %) was observed for ADC, D, f and T2* measured over the whole kidney. Hydralazine induced a marked and significant (p < 0.05) reduction in whole kidney ADC, D, and T2*, and a significant (p < 0.05) increase in D* and f. Furosemide significantly (p < 0.05) increased whole kidney ADC, D, and T2*. A more variable response to angiotensin II was determined, with a significant (p < 0.05) increase in medulla D* and significant (p < 0.05) reduction in whole kidney T2* established.ConclusionsMultiparametric MRI, incorporating quantitation of IVIM DWI and BOLD biomarkers and performed on a clinical platform, can be used to monitor the acute effects of vascular and tubular modulating drugs on rat kidney function in vivo. Clinical adoption of such functional imaging biomarkers can potentially inform on treatment effects in patients with renal dysfunction.Electronic supplementary materialThe online version of this article (doi:10.1186/s12882-016-0356-x) contains supplementary material, which is available to authorized users.

Nigella sativa oil attenuates chronic nephrotoxicity induced by oral sodium nitrite: Effects on tissue fibrosis and apoptosis

Objectives: Sodium nitrite, a food preservative, has been reported to increase oxidative stress indicators such as lipid peroxidation, which can affect different organs including the kidney. Here, we investigated the toxic effects of oral sodium nitrite on kidney function in rats and evaluated potential protective effects of Nigella sativa oil (NSO). Methods: Seventy adult male Sprague–Dawley rats received 80 mg/kg sodium nitrite orally in the presence or absence of NSO (2.5, 5, and 10 ml/kg) for 12 weeks. Morphological changes were assessed by hematoxylin and eosin, Mallory trichome, and periodic acid–Schiff staining. Renal tissues were used for measurements of oxidative stress markers, C-reactive protein, cytochrome C oxidase, transforming growth factor (TGF)-beta1, monocyte chemotactic protein (MCP)-1, pJNK/JNK, and caspase-3. Results: NSO significantly reduced sodium nitrite-induced elevation in serum urea and creatinine, as well as increasing normal appearance of renal tissue. NSO also prevented reductions in glycogen levels caused by sodium nitrite alone. Moreover, NSO treatment resulted in dose-dependent significant reductions in fibrosis markers after sodium nitrite-induced 3- and 2.7-fold increase in MCP-1 and TGF-beta1, respectively. Finally, NSO partially reduced the elevated caspase-3 and pJNK/JNK. Discussion: NSO ameliorates sodium nitrite-induced nephrotoxicity through blocking oxidative stress, attenuation of fibrosis/inflammation, restoration of glycogen level, amelioration of cytochrome C oxidase, and inhibition of apoptosis.

Impact of combined treatment with rosuvastatin and antidepressants on liver and kidney function in rats.

Depression is among the most prevalent and life-threatening forms of mental illness, and is also a risk factor for cardiovascular disorders, diabetes and metabolic syndrome. Elderly patients commonly receive statins for the prevention of cardiovascular diseases, and antidepressant drugs for the treatment of depression. It should be noted that long-term polypharmacotherapy may lead to potential drug interactions and disorders of the organs. The aim of the present study was to determine whether, and to what extent, combined treatment with rosuvastatin and antidepressants (amitriptyline or fluoxetine) influences the biochemical markers of liver and kidney function in a rat model. For this purpose, the activity levels of aspartate aminotransferase, alanine aminotransferase (ALT), γ-glutamyltransferase (GGT) and the concentrations of total protein, urea, creatinine and β2-microglobulin were determined. The results of the study indicated that combined treatment with rosuvastatin and the antidepressants amitriptyline and fluoxetine for 14 days altered the activity levels of ALT and GGT, and the concentrations of urea and creatinine in the serum compared with groups of rats receiving rosuvastatin or either antidepressant alone. These observed changes in biochemical parameters may suggest the possibility of impaired liver and kidney function during the continuous combined exposure to the drugs. However, further clinical and animal studies are required in order to further elucidate this process.

Metabolic acidosis aggravates experimental acute kidney injury

AimsIschemia/reperfusion (I/R) injury and metabolic acidosis (MA) are two critical conditions that may simultaneously occur in clinical practice. The result of this combination can be harmful to the kidneys, but this issue has not been thoroughly investigated. The present study evaluated the influence of low systemic pH on various parameters of kidney function in rats that were subjected to an experimental model of renal I/R injury. Main methodsMetabolic acidosis was induced in male Wistar rats by ingesting ammonium chloride (NH4Cl) in tap water, beginning 2days before ischemic insult and maintained during the entire study. Ischemia/reperfusion was induced by clamping both renal arteries for 45min, followed by 48h of reperfusion. Four groups were studied: control (subjected to sham surgery, n=8), I/R (n=8), metabolic acidosis (MA; 0.28M NH4Cl solution and sham surgery, n=6), and MA+I/R (0.28M NH4Cl solution plus I/R, n=9). Key findingsCompared with I/R rats, MA+I/R rats exhibited higher mortality (50 vs. 11%, p=0.03), significant reductions of blood pH, plasma bicarbonate (pBic), and standard base excess (SBE), with a severe decline in the glomerular filtration rate and tubular function. Microscopic tubular injury signals were detected. Immunofluorescence revealed that the combination of MA and I/R markedly increased nuclear factor κB (NF-κB) and heme-oxygenase 1 (HO-1), but it did not interfere with the decrease in endothelial nitric oxide synthase (eNOS) expression that was caused by I/R injury. SignificanceAcute ischemic kidney injury is exacerbated by acidic conditions.

The protective effect of Nigella sativa against cisplatin-induced nephrotoxicity in rats.

The clinical use of cisplatin is highly restricted, because of its nephrotoxicity. In this study the protective effect of Nigella sativa (N. sativa) against cisplatin-induced nephrotoxicity was investigated in rats. In the current study, the effects of the administration of aqueous-ethanolic extract of N. sativa (100 and 200 mg/kg, BW) and vitamin E (100 mg/kg, BW) against blood and urine biochemical alterations and kidney function in rats treated with cisplatin were investigated. Cisplatin was injected at a dose of 6 mg/kg, BW, on the sixth day of the experiment. The results indicated significant changes in serum urea and creatinine concentration, urine glucose concentration, and urine output in cisplatin group compared with control group. Serum urea and creatinine concentration in preventive and preventive+treatment vitamin E and preventive+treatment N. sativa (200 mg/kg, BW) groups and also serum creatinine concentration in preventive+treatment N. sativa (100 mg/kg, BW) group significantly decreased compared with cisplatin group. Urine glucose concentration in preventive and preventive+treatment N. sativa groups and urine output in preventive and preventive+treatment N. sativa (200 mg/kg, BW) groups significantly decreased compared with cisplatin group.Osmolarity excretion rate in preventive and preventive+treatment vitamin E and preventive N. sativa groups was significantly higher than control group. The current study suggests that N. sativa extract and vitamin E in a dose- and time-dependent manner improved the serum and urine biochemical parameters and kidney function in cisplatin-induced nephrotoxicity in rats. However, it needs more investigations to determine the mechanism of N. sativa action on cisplatin-induced kidney toxicity.

Effect of acute and chronic treatment of Cyclosporin A on liver and kidney functions in rats

Comparative effect of chronic administration of chloroquine phosphate and methanol extract of Landolphia owariensis on the activities of rat EnzymesIlesanmi F F, Balogun E A, Ilesanmi O S

Acute effects of grayanotoxin in rhododendron honey on kidney functions in rats.

The aim of the study is to evaluate the acute biochemical and histological changes in rat kidneys after treatment with grayanotoxin (GTX) of rhododendron honey (RH). A total of 60 Sprague-Dawley female rats were divided into five groups of 12 rats each, one being a control group (group 1) and group 2 was treated with 0.015 mg/kg/bw of GTX standard preparation via intraperitoneal injection. Groups 3, 4, and 5 were given RH at doses of 0.1, 0.5, and 2.5 g/kg/bw, respectively, via oral gavage. Compared to the control group, significant increases were observed in glucose, blood urea nitrogen (BUN), and creatinine levels of the GTX-injected groups after 1 h. However, in low dose RH group, such an increase was not observed and had a normal appearance histologically. Therefore, low dose (1 g/kg/bw) of RH produces no acute adverse effects on renal functions of rats.

Ameliorating effects of goby fish protein hydrolysates on high-fat-high-fructose diet-induced hyperglycemia, oxidative stress and deterioration of kidney function in rats

This study investigated the therapeutic potential of undigested goby fish (Zosterisessor ophiocephalus) muscle proteins (UGP) and their hydrolysates on high-fat-high-fructose diet (HFFD)-fed rats.HFFD induced hyperglycemia, manifested by a significant increase in the levels of glucose and glycogen as well as α-amylase activity when compared to normal rats. The administration of GPHs to HFFD-fed rats significantly decreased α-amylase activity and the contents of blood glucose and hepatic glycogen. By contrast, the UGP increased the glucose metabolic disorders in HFFD-fed rats.Furthermore, HFFD-fed rats showed oxidative stress, as evidenced by decreased antioxidant enzyme activities and glutathione (GSH) levels and increased concentration of the lipid peroxidation product malondialdehyde in liver and kidney. Interestingly, the daily gavage of UGP and GPHs improved the redox status in liver and kidney of HFFD-rats by ameliorating or reversing the above-mentioned changes. Moreover, GPHs exhibited a renal protective role by reversing the HFFD-induced decease of uric acid and increase of creatinine levels in serum and preventing some HFFD-induced changes in kidney architecture. The results demonstrate that GPHs contain bioactive peptides that possess significant hypoglycemic and antioxidant properties, and ameliorate renal damage in rats fed hypercaloric diet.

Neural regulation of the kidney function in rats with cisplatin induced renal failure.

Aim: Chronic kidney disease (CKD) is often associated with a disturbed cardiovascular homeostasis. This investigation explored the role of the renal innervation in mediating deranged baroreflex control of renal sympathetic nerve activity (RSNA) and renal excretory function in cisplatin-induced renal failure.Methods: Rats were either intact or bilaterally renally denervated 4 days prior to receiving cisplatin (5 mg/kg i.p.) and entered a chronic metabolic study for 8 days. At day 8, other groups of rats were prepared for acute measurement of RSNA or renal function with either intact or denervated kidneys.Results: Following the cisplatin challenge, creatinine clearance was 50% lower while fractional sodium excretion and renal cortical and medullary TGF-β1 concentrations were 3–4 fold higher in both intact and renally denervated rats compared to control rats. In cisplatin-treated rats, the maximal gain of the high-pressure baroreflex curve was only 20% that of control rats, but following renal denervation not different from that of renally denervated control rats. Volume expansion reduced RSNA by 50% in control and in cisplatin-treated rats but only following bilateral renal denervation. The volume expansion mediated natriuresis/diuresis was absent in the cisplatin-treated rats but was normalized following renal denervation.Conclusions: Cisplatin-induced renal injury impaired renal function and caused a sympatho-excitation with blunting of high and low pressure baroreflex regulation of RSNA, which was dependent on the renal innervation. It is suggested that in man with CKD there is a dysregulation of the neural control of the kidney mediated by its sensory innervation.

Protective effect of kombucha on rats fed a hypercholesterolemic diet is mediated by its antioxidant activity

Context: Kombucha (KT) is claimed to have various beneficial effects on human health, but there is very little scientific evidence available in the literature.Objective: The present study investigates the effects of Camellia sinensis (GT) Linn. (Theaceae) and KT, two natural drinks, on cholesterol and antioxidant status using a hypercholesterolemia rat model.Materials and methods: The present study compared the free-radical scavenging abilities and polyphenol levels of GT and KT. Wistar rats fed cholesterol-rich diets were given KT or GT (5 mL/kg body weight per day, po) for 16 weeks, then fasted overnight and sacrificed. The plasma lipid levels, thiobarbituric acid reactive substances (TBARS) and aspartate aminotransferase (AST), alanine aminotransferase (ALT), and γ-glutamyl transpeptidase (GGT) serum levels, antioxidant activities of superoxide dismutase (SOD) and catalase (CAT), and creatinine and urea rats were examined.Results: KT had a phenolic compound of 955 ± 0.75 mg GAE/g) followed, by GT (788.92 ± 0.02 mg GAE/g). The free radical scavenging activity of KT was higher than GT. Compared with GT, KT induced lowered serum levels of TC, TG, VLDL-C, and LDL-C by 26, 27, 28, and 36%, respectively, and increased the serum level of high-density lipoprotein cholesterol (HDL-C). KT induced a 55% decrease of TBARS level in liver and 44% in kidney, compared with those of rats fed a cholesterol-rich diet alone. Moreover, CAT and SOD activities were reduced by 29 and 33%, respectively, in liver and 31 and 35%, respectively, in kidney, after oral administration of KT, compared with those of HCD-fed rats.Conclusion: The findings revealed that KT administration induced attractive curative effects on hypercholesterolemic, particularly in terms of liver–kidney functions in rats. Its effect on humans needs to be studied further.

The adverse effects of long-terml-carnitine supplementation on liver and kidney function in rats

Levo-Carnitine (l-carnitine) is widely used in health and food. This study was to focus on the adverse effects of 8-week oral supplementation of l-carnitine (0.3 and 0.6 g/kg) in female and male Sprague Dawley rats. l-carnitine reduced body and fat weights, as well as serum, liver, and kidney lipid levels in rats. Simultaneously, hepatic fatty acid β-oxidation and lipid synthesis were disturbed in l-carnitine-fed rats. Moreover, l-carnitine accelerated reactive oxygen species production in serum and liver, thereby triggering hepatic NOD-like receptor 3 (NLRP3) inflammasome activation to elevate serum interleukin (IL)-1β and IL-18 levels in rats. Alteration of serum alkaline phosphatase levels further confirmed liver dysfunction in l-carnitine-fed rats. Additionally, l-carnitine may potentially disturb kidney function by altering renal protein levels of rat organic ion transporters. These observations may provide the caution information for the safety of long-term l-carnitine supplementation.

Effect of low carbohydrate high protein (LCHP) diet on lipid metabolism, liver and kidney function in rats

The objective of this study was to compare effects of Western diet (WD) with low carbohydrate high protein (LCHP) diet on lipid metabolism, liver and kidney function in rats. Eighteen rats were randomly assigned to three experimental groups and fed for the next 2 months. The experimental diets were: Control (7% of soybean oil, 20% protein), WD (21% of butter, 20% protein), and LCHP (21% of butter and 52.4% protein) diet. The LCHP diet significantly decreased the body weight of the rats. Diet consumption was differentiated among groups, however significant changes were observed since third week of the experiment duration. Rats fed LCHP diet ate significantly less (25.2g/animal/day) than those from Control (30.2g/animal/day) and WD (27.8g/animal/day) groups. Additionally, food efficiency ratio (FER) tended to decrease in LCHP fed rats. Serum homocysteine concentration significantly decreased in rats fed WD and LCHP diets. Liver weights were significantly higher in rats fed WD and LCHP diets. At the end of the experiment (2 months) the triacylglycerol (TAG) was significantly decreased in animals fed LCHP compared to WD. qRT-PCR showed that SCD-1 and FAS were decreased in LCHP fed rats, but WD diet increased expression of lipid metabolism genes. Rats receiving LCHP diet had two fold higher kidney weight and 54.5% higher creatinin level compared to Control and WD diets. In conclusion, LCHP diet decreased animal's body weight and decreased TAG in rat's serum. However, kidney damage in LCHP rats was observed.

Effects of Dietary Calcium Supplementation on Bone Metabolism, Kidney Mineral Concentrations, and Kidney Function in Rats Fed a High-Phosphorus Diet.

We investigated the effects of dietary calcium (Ca) supplementation on bone metabolism, kidney mineral concentrations, and kidney function in rats fed a high-phosphorus (P) diet. Wistar strain rats were randomly divided into 4 dietary groups and fed their respective diets for 21 d: a diet containing 0.3% P and 0.5% Ca (C), a diet containing 1.5% P and 0.5% Ca (HP), a diet containing 0.3% P and 1.0% Ca (HCa), or a diet containing 1.5% P and 1.0% Ca (HPCa). Compared to the C group, the high-P diet increased serum parathyroid hormone concentration, markers of bone turnover, receptor activator of NF-κB ligand mRNA expression of the femur, kidney Ca and P concentrations, urinary N-acetyl-β-D-glucosaminidase activity, and urinary β2-microglobulin excretion, and decreased bone mineral content and bone mineral density of the femur and tibia. Dietary Ca supplementation improved the parameters of bone metabolism and kidney function in rats fed the high-P diet, while there were no significant differences in kidney Ca or P concentrations between the HP and HPCa groups. These results suggest that dietary Ca supplementation prevented the bone loss and decline in kidney function induced by a high-P diet, whereas dietary Ca supplementation did not affect kidney mineral concentrations in rats fed the high-P diet.

Hepatorenal Protective Activities of Plantain Root (Musa paradisiaca) on Arsenic-induced Oxidative Damage in Rat

The protective role of aqueous root extract of Musa paradisiaca on arsenic chloride-induced oxidative damage in the liver and kidney of albino rats was investigated in this study. Twenty four albino rats were grouped in to four (A, B, C and D). Group A served as the control and received distilled water while B, C and D were administered 10 mg/kg bw of arsenic chloride weekly. Groups C and D were treated with 200 and 500 mg/kg bw of aqueous extract of Musa paradisiaca roots respectively for 28 days while group B was left untreated. Phytochemical screening carried out on the root powder indicated the presence of tannins, terpenoids, steroids, sarponins, cardiac glycosides and flavonoids. Arsenic chloride induced a significant elevation in aminotransferases (ALT and AST), ALP and total bilirubin and reduction in serum protein and albumin indicating derangement of liver function. Significant elevation of serum creatinine, urea, uric acid, blood urea nitrogen and electrolytes levels were also recorded in arsenic intoxicated rats indicating disruption of kidney function. Histological examination of the kidney and liver of arsenic intoxicated rats also indicated significant alteration in tissue architecture and morphology. There was significant increase in the liver and kidney weight index in arsenic treated groups compared to the control indicating tissue inflammation. Treatment of rats with different doses of Musa paradisiaca root extract significantly (P<0.05) normalized liver and kidney functions while it also restored normal tissue histology at the end of the experiment. It can be concluded that Musa paradisiaca contain bioactive constituents capable of protecting the living system against arsenic-induced disruption of liver and kidney functions in rats.