scholarly journals Effects ofBauhinia forficataTea on Oxidative Stress and Liver Damage in Diabetic Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Andréia Caroline Fernandes Salgueiro ◽  
Vanderlei Folmer ◽  
Marianne Pires da Silva ◽  
Andreas Sebastian Loureiro Mendez ◽  
Ana Paula Pegoraro Zemolin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Body Weight ◽  
Liver Damage ◽  
Weight Ratio ◽  
Protein Carbonyl ◽  
Diabetic Mice ◽  
Body Weight Ratio ◽  
Glucose Levels ◽  
Nonprotein Thiols

This study was designed to evaluate the effects ofBauhinia forficataLink subsp.pruinosa(BF) tea on oxidative stress and liver damage in streptozotocin (STZ)-induced diabetic mice. Diabetic male mice have remained 30 days without any treatment. BF treatment started on day 31 and continued for 21 days as a drinking-water substitute. We evaluated (1) BF chemical composition; (2) glucose levels; (3) liver/body weight ratio and liver transaminases; (4) reactive oxygen species (ROS), lipid peroxidation, and protein carbonylation in liver; (5) superoxide dismutase (SOD) and catalase (CAT) activities in liver; (6)δ-aminolevulinate dehydratase (δ-ALA-D) and nonprotein thiols (NPSH) in liver; (7) Nrf2, NQO-1, and HSP70 levels in liver and pancreas. Phytochemical analyses identified four phenols compounds. Diabetic mice present high levels of NQO-1 in pancreas, increased levels of ROS and lipid peroxidation in liver, and decrease in CAT activity. BF treatment normalized all these parameters. BF did not normalize hyperglycemia, liver/body weight ratio, aspartate aminotransferase, protein carbonyl, NPSH levels, andδ-ALA-D activity. The raised oxidative stress seems to be a potential mechanism involved in liver damage in hyperglycemic conditions. Our results indicated that BF protective effect could be attributed to its antioxidant capacity, more than a hypoglycemic potential.

scholarly journals Creatine Alleviates Doxorubicin-Induced Liver Damage by Inhibiting Liver Fibrosis, Inflammation, Oxidative Stress, and Cellular Senescence

Nutrients ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 41
Author(s):  
Nouf Aljobaily ◽  
Michael J. Viereckl ◽  
David S. Hydock ◽  
Hend Aljobaily ◽  
Tsung-Yen Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Methylation ◽  
Body Weight ◽  
Liver Fibrosis ◽  
Liver Damage ◽  
Cellular Senescence ◽  
Weight Ratio ◽  
Mrna Levels ◽  
Body Weight Ratio ◽  
Chromosomal Stability

Background: Treatment with the chemotherapy drug doxorubicin (DOX) may lead to toxicities that affect non-cancer cells including the liver. Supplementing the diet with creatine (Cr) has been suggested as a potential intervention to minimize DOX-induced side effects, but its effect in alleviating DOX-induced hepatoxicity is currently unknown. Therefore, we aimed to examine the effects of Cr supplementation on DOX-induced liver damage. Methods: Male Sprague-Dawley rats were fed a diet supplemented with 2% Cr for four weeks, 4% Cr for one week followed by 2% Cr for three more weeks, or control diet for four weeks. Animals then received either a bolus i.p. injection of DOX (15 mg/kg) or saline as a placebo. Animals were then sacrificed five days-post injection and markers of hepatoxicity were analyzed using the liver-to-body weight ratio, aspartate transaminase (AST)-to- alanine aminotransferase (ALT) ratio, alkaline phosphatase (ALP), lipemia, and T-Bilirubin. In addition, hematoxylin and eosin (H&E) staining, Picro-Sirius Red staining, and immunofluorescence staining for CD45, 8-OHdG, and β-galactosidase were performed to evaluate liver morphology, fibrosis, inflammation, oxidative stress, and cellular senescence, respectively. The mRNA levels for biomarkers of liver fibrosis, inflammation, oxidative stress, and senescence-related genes were measured in liver tissues. Chromosomal stability was evaluated using global DNA methylation ELISA. Results: The ALT/AST ratio and liver to body weight ratio tended to increase in the DOX group, and Cr supplementation tended to attenuate this increase. Furthermore, elevated levels of liver fibrosis, inflammation, oxidative stress, and senescence were observed with DOX treatment, and Cr supplementation prior to DOX treatment ameliorated this hepatoxicity. Moreover, DOX treatment resulted in chromosomal instability (i.e., altered DNA methylation profile), and Cr supplementation showed a tendency to restore chromosomal stability with DOX treatment. Conclusion: The data suggest that Cr protected against DOX-induced hepatotoxicity by attenuating fibrosis, inflammation, oxidative stress, and senescence.

Abstract 229: Increased Ace Gene Dosage Reduces Ace2 Activity in Diabetic Mice Kidney: Involvement of Ace/ace2 Balance on the Development of Diabetic Nephropathy

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Nadia S Bertoncello ◽  
Roseli P Moreira ◽  
Rodrigo Yokota ◽  
Rodolfo M Rosa ◽  
Danielle Y Arita ◽  
...  
Keyword(s):  
Body Weight ◽  
Diabetic Nephropathy ◽  
Gene Dosage ◽  
Weight Ratio ◽  
Gene Copy ◽  
Diabetic Mice ◽  
Body Weight Ratio ◽  
Ace Gene ◽  
Kidney Involvement ◽  
Ace Activity

The mechanisms underlying the link between high constitutive levels of ACE and diabetic nephropathy has not been completely understood, but an imbalance between angiotensin I (ACE) and II (ACE2) converting enzymes homeostasis has been described in diabetic kidney disease. The aim of this study was to evaluate ACE/ACE2 homeostasis in kidney from diabetic mice presenting increased dosage of ACE gene. Male mice (3 months old) genetically engineered to harbor one or three copies of the ACE gene were made diabetic (streptozotocin - STZ, 50 mg/Kg) and randomly assigned into: 1-copy control (1CC), 1-copy diabetic (1CD), 3-copy control (3CC) and 3-copy diabetic. At the end of experimental period body weight was evaluated and kidney was excised. Kidney-to-body weight ratio and ACE and ACE 2 activities were determined using specific substrates (ZPhe-HL and 7-Mca-APK(Dnp), respectively) (Two way ANOVA + Tukey test; P<0.05). Diabetes increased blood glucose (1CD : 436 ± 25 vs. 1CC: 90 ± 2; 3CD: 556 ± 6 vs. 3CC: 112 ± 4 mg/dL) and kidney-to-body weight ratio (1CD: 7.5 ± 0.2 vs. 1CC: 5.8 ± 0.2; 3CD: 7.8 ± 0.1 vs. 3CC: 5.8 ± 0.1 mg/g) with no influence of ACE genotype. As expected, renal ACE activity was directly related to ACE gene copy number in control group (3CC: 9.4 ± 2.11 vs. 1CC:5.6 ± 0.9 mU/mg protein). Renal ACE activity was decreased in diabetic groups (1CD: 3.6 ± 0.2 vs. 1CC: 5.6 ± 0.9; 3CD: 2.3 ± 0.4 vs. 3CC: 9.4 ± 2.1 mU/mg protein) with no influence of ACE genotype. Under physiological condition, renal ACE2 activity remained unchanged regardless of the ACE genotype (1CC: 1.9 ± 0.2 = 3CC: 1.4 ± 0.1 μM/min/mg). However upon a pathological stimulus, renal ACE2 activity was efficiently increased only in 1CD group, but not in 3CD, as compared with the others (1CD: 5.1 ± 0.9 vs. 1CC: 1.9 ± 0.2 = 3CC: 1.4 ± 0.1 = 3CD: 2.2 ± 0.2 μM/min/mg). Taken together, our results show for the first time, that susceptibility for the development of diabetic nephropathy associated with increased ACE gene dosage may be, at least in part, caused by a decrease on renal ACE2 activity. This may result in increased local levels of angiotensin II and decreased angiotensin (1-7), leading to altered glomerular permeability and albuminuria, functional alterations presented by 3CD animals. Financial Support: FAPESP, CAPES, CNPq.

The effects of oral glutamine on cyclophosphamide-induced nephrotoxicity in rats

2010 ◽  
Vol 30 (7) ◽  
pp. 616-623 ◽  
Author(s):  
Premila Abraham ◽  
Bina Isaac
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Body Weight ◽  
Renal Damage ◽  
Neutrophil Infiltration ◽  
Protein Carbonyl ◽  
Male Rats ◽  
Glutathione Depletion ◽  
Myeloperoxidase Activity ◽  
Protein Carbonyl Content

Nephrotoxicity is one of the adverse side effects of cyclophosphamide (CP) chemotherapy. In a recent study, we have demonstrated that oxidative stress and glutathione depletion play important roles in CP-induced renal damage. The aim of the study was to verify whether glutamine, the precursor for glutathione synthesis, prevents CP-induced oxidative stress and renal damage using a rat model. Adult male rats were administered a single dose of 150 mg/ kg body weight of CP intraperitoneally. The glutamine-pretreated rats were administered 1 gm/kg body weight of glutamine orally 2 h before the administration of CP. Vehicle/glutaminetreated rats served as controls. All the rats were killed 16 h after the dose of CP/vehicle. The kidneys were removed and used for light microscopic and biochemical studies. The markers of oxidative stress including malondialdehyde content, protein carbonyl content, protein thiol, reduced glutathione and myeloperoxidase activity, a marker of neutrophil infiltration, were measured in kidney homogenates. CP treatment-induced damage to kidney involved the glomeruli and the tubules. Pretreatment with glutamine reduced CP-induced glutathione depletion and increased myeloperoxidase activity. However, it did not prevent CP-induced lipid peroxidation, protein carbonylation and renal damage. The results of the present study suggest that glutamine pretreatment does not prevent CP-induced lipid peroxidation and renal damage, although it prevents CP-induced glutathione depletion and neutrophil infiltration significantly. It is suggested that mechanisms other than oxidative stress may also be involved and/or oxidative stress may be consequence and not the cause of CP induced renal damage.

scholarly journals ADAMTS13/VWF Axis Potentially Contributes to Diabetic Nephropathy By Regulating PAI-1 Levels

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 2240-2240
Author(s):  
Nirav Dhanesha ◽  
Anil K. Chauhan
Keyword(s):  
Body Weight ◽  
Diabetic Nephropathy ◽  
Renal Injury ◽  
Weight Ratio ◽  
Diabetic Patients ◽  
Diabetic Mice ◽  
Body Weight Ratio ◽  
Renal Hypertrophy ◽  
Protein Levels ◽  
Pai 1

Abstract Background and objective: ADAMTS13 (A Disintegrin And Metalloprotease with Thrombospondin type I repeats-13) cleaves von Willebrand factor (VWF), a large multimeric protein that plays an important role in hemostasis and thrombosis. Severe deficiency or very low levels of ADAMTS13 in presence of external stimuli results in accumulation of thrombogenic ultra large VWF multimers (which are released from activated endothelium) known to trigger thrombotic microangiopathy. Activated endothelium/dysfunction is a prominent feature of diabetic nephropathy, and advanced diabetic glomerulopathy often exhibits thrombotic microangiopathy. Significantly reduced ADAMTS13 and increased plasma VWF levels have been found in diabetic patients with nephropathy. Although major site of ADAMTS13 synthesis is liver, ADAMTS13 is also expressed by podocytes in normal renal cortex. It remains unknown, however, whether VWF and ADAMTS13 imbalance plays a causal role in development of nephropathy in diabetic patients or rather is simply an associate marker of disease status, possibly secondary to endothelial function. We performed experiments in genetic models to determine whether ADAMTS13 and VWF axis contributes to diabetic nephropathy. Methods : Male, 8-10 weeks old wild-type (WT), Adamts13-/- and Vwf-/- mice were made diabetic by injecting multiple low doses of streptozotocin (60 mg/kg, i.p. for five consecutive days). Successful diabetes induction was tested after 2 weeks by measuring blood glucose. Mice having blood glucose levels above 300 mg/dL were included in the study. Controls were nondiabetic littermate mice treated with citrate buffer. The extent of renal injury was evaluated after 28 weeks of diabetes induction by measuring albuminuria and kidney to body weight ratio. Renal hypertrophy and extracellular matrix deposition was quantified by hematoxylin and immunostaining. PAI-1 mRNA and protein levels were measured by real time quantitative RT-PCR and ELISA. Results: Adamts13- /- diabetic mice exhibited significantly increased kidney to body weight ratio (P<0.05 vs. WT diabetic mice). Urine albuminuria, an index of renal injury was significantly elevated in Adamts13-/- diabetic mice (P<0.05 vs. WT diabetic mice). Increased renal injury in Adamts13-/- diabetic mice was concomitant with increased renal hypertrophy and extracellular matrix (ECM) deposition within glomeruli (P<0.05 vs. WT diabetic mice). Murine studies have shown that PAI-1 contributes to diabetic nephropathy by regulating TGF-beta and ECM deposition. A positive association exists between increased PAI-1 levels in glomeruli and microangiopathy in patients with diabetic nephropathy. We determined whether ADAMTS13 deficiency-induced microangiopathy in glomeruli increases PAI-1 levels. Adamts13-/- diabetic mice exhibited increased PAI-1 mRNA and protein levels (P<0.05 vs. WT diabetic mice). VWF remains the only known substrate of ADAMTS13 and increased plasma VWF levels have been associated with diabetic nephropathy. We determined the role of VWF in diabetic nephropathy. Vwf-/- diabetic mice exhibited significantly decreased kidney weight/body weight ratio, less urinary albuminuria, decreased kidney PAI-1 expression levels concomitant with improved kidney morphological changes (P<0.05 vs. WT diabetic mice). Conclusion : These findings provide experimental evidence for the first time that ADAMTS13/VWF axis potentially contributes to diabetic nephropathy, most likely by regulating PAI-1 levels. Disclosures No relevant conflicts of interest to declare.

scholarly journals Lipoic Acid Exacerbates Oxidative Stress and Lipid Accumulation in the Liver of Wistar Rats Fed a Hypercaloric Choline-Deficient Diet

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1999
Author(s):  
Lidia V. Kravchenko ◽  
Ilya V. Aksenov ◽  
Nikolay S. Nikitin ◽  
Galina V. Guseva ◽  
Ludmila I. Avrenyeva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Liver Disease ◽  
Lipoic Acid ◽  
Lipid Accumulation ◽  
Wistar Rats ◽  
Weight Ratio ◽  
Body Weight Ratio ◽  
Deficient Diet ◽  
Male Wistar Rats

Non-alcoholic fatty liver disease (NAFLD) is currently estimated as the most prevalent chronic liver disease in all age groups. An increasing body of evidence obtained in experimental and clinical data indicates that oxidative stress is the most important pathogenic factor in the development of NAFLD. The study aimed to investigate the impact of α-lipoic acid (LA), widely used as an antioxidant, on the effects of a hypercaloric choline-deficient diet. Male Wistar rats were divided into three groups: control diet (C); hypercaloric choline-deficient diet (HCCD), and hypercaloric choline-deficient diet with α-lipoic acid (HCCD+LA). Supplementation of HCCD with LA for eight weeks led to a decrease in visceral adipose tissue/body weight ratio, the activity of liver glutathione peroxidase and paraoxonase-1, plasma, and liver total antioxidant activity, as well as an increase in liver/body weight ratio, liver total lipid and triglyceride content, and liver transaminase activities compared to the HCCD group without LA. In conclusion, our study shows that α-lipoic acid detains obesity development but exacerbates the severity of diet-induced oxidative stress and lipid accumulation in the liver of male Wistar rats fed a hypercaloric choline-deficient diet.

scholarly journals Comparison of the obesity phenotypes related to monosodium glutamate effect on arcuate nucleus and/or the high fat diet feeding in C57Bl/6 and NMRI mice

2008 ◽  
pp. 727-734
Author(s):  
R Matyšková ◽  
L Maletínská ◽  
J Maixnerová ◽  
Z Pirník ◽  
A Kiss ◽  
...  
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Arcuate Nucleus ◽  
Monosodium Glutamate ◽  
Weight Ratio ◽  
High Fat ◽  
Body Weight Ratio ◽  
Nmri Mice ◽  
Glucose Levels ◽  
Diet Induced Obesity

In this study, susceptibility of inbred C57BL/6 and outbred NMRI mice to monosodium glutamate (MSG) obesity or diet-induced obesity (DIO) was compared in terms of food intake, body weight, adiposity as well as leptin, insulin and glucose levels. MSG obesity is an early-onset obesity resulting from MSGinduced lesions in arcuate nucleus to neonatal mice. Both male and female C57BL/6 and NMRI mice with MSG obesity did not differ in body weight from their lean controls, but had dramatically increased fat to body weight ratio. All MSG obese mice developed severe hyperleptinemia, more remarkable in females, but only NMRI male mice showed massive hyperinsulinemia and an extremely high HOMA index that pointed to development of insulin resistance. Diet-induced obesity is a late-onset obesity; it developed during 16-week-long feeding with high-fat diet containing 60 % calories as fat. Inbred C57BL/6 mice, which are frequently used in DIO studies, both male and female, had significantly increased fat to body weight ratio and leptin and glucose levels compared with their appropriate lean controls, but only female C57BL/6 mice had also significantly elevated body weight and insulin level. NMRI mice were less prone to DIO than C57BL/6 ones and did not show significant changes in metabolic parameters after feeding with high-fat diet.

Effect of taxifolin/dapagliflozin combination on colistin-induced nephrotoxicity in rats

2021 ◽  
pp. 096032712110109
Author(s):  
AM Kabel ◽  
SA Salama
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Growth Factor ◽  
Weight Ratio ◽  
Nuclear Factor ◽  
Body Weight Ratio ◽  
Kidney Weight ◽  
Oxidative Stress Parameters ◽  
Tgf Β1 ◽  
Stress Parameters

Colistin is an antimicrobial agent that is used in resistant gram-negative infections. Its most common dose-limiting adverse effect is nephrotoxicity. The objective of our study was to explore the possible effects of each of taxifolin and dapagliflozin alone and in combination on colistin-induced nephrotoxicity in rats. Sixty male rats were randomized into six groups: Control; colistin; colistin + taxifolin; colistin + dapagliflozin; colistin + carboxymethyl cellulose (CMC) and colistin + taxifolin + dapagliflozin. Dapagliflozin, taxifolin, and CMC were given daily for 7 days, 4 hours before colistin injection. Kidney weight/body weight ratio and renal function tests were determined. Renal tissue nerve growth factor-β (NGF-β), transforming growth factor beta 1 (TGF-β1), proinflammatory cytokines, nuclear factor (erythroid-derived 2)-like 2 (Nrf2), toll-like receptor 4 (TLR4), nuclear factor kappa B (NF-κB) p65, signal transducer and activator of transcription 3 (STAT3), oxidative stress parameters, beclin-1 and c-Jun NH2-terminal kinase (JNK) activities were measured. Kidneys were examined histopathologically and immunohistochemically. Taxifolin and/or dapagliflozin induced significant improvement in the renal functions and oxidative stress parameters with significant increase in tissue Nrf2, STAT3 and NGF-β accompanied with significant decrease in kidney weight/body weight ratio, tissue proinflammatory cytokines, TGF-β1, NF-κB (p65), TLR4, beclin-1 and JNK activities and improved the histopathological picture when compared to rats treated with colistin alone. This improvement was significant with taxifolin/dapagliflozin combination compared to rats treated with each of these agents alone. So, we concluded that the combined use of taxifolin and dapagliflozin may confer a therapeutic tool for attenuation of colistin-induced nephrotoxicity.

scholarly journals Chronic Hyperinsulinaemic Hypoglycaemia in Rats Is Accompanied by Increased Body Weight, Hyperleptinaemia, and Decreased Neuronal Glucose Transporter Levels in the Brain

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Vivi F. H. Jensen ◽  
Anne-Marie Mølck ◽  
Melissa Chapman ◽  
Lene Alifrangis ◽  
Lene Andersen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Body Weight ◽  
Food Consumption ◽  
Glucose Transporter ◽  
Redox Homeostasis ◽  
Hyperinsulinaemic Hypoglycaemia ◽  
Lipid Peroxidation Products ◽  
Glucose Levels ◽  
The Brain

The brain is vulnerable to hypoglycaemia due to a continuous need of energy substrates to meet its high metabolic demands. Studies have shown that severe acute insulin-induced hypoglycaemia results in oxidative stress in the rat brain, when neuroglycopenia cannot be evaded despite increased levels of cerebral glucose transporters. Compensatory measures in the brain during chronic insulin-induced hypoglycaemia are less well understood. The present study investigated how the brain of nondiabetic rats copes with chronic insulin-induced hypoglycaemia for up to eight weeks. Brain level of different substrate transporters and redox homeostasis was evaluated. Hyperinsulinaemia for 8 weeks consistently lowered blood glucose levels by 30–50% (4–6 mM versus 7–9 mM in controls). The animals had increased food consumption, body weights, and hyperleptinaemia. During infusion, protein levels of the brain neuronal glucose transporter were decreased, whereas levels of lipid peroxidation products were unchanged. Discontinued infusion was followed by transient systemic hyperglycaemia and decreased food consumption and body weight. After 4 weeks, plasma levels of lipid peroxidation products were increased, possibly as a consequence of hyperglycaemia-induced oxidative stress. The present data suggests that chronic moderate hyperinsulinaemic hypoglycaemia causes increased body weight and hyperleptinaemia. This is accompanied by decreased neuronal glucose transporter levels, which may be leptin-induced.

scholarly journals Ameliorative Effect of Chlorophyllin on Oxidative Stress in Experimental Model of Diabetes

2017 ◽  
Vol 8 (4) ◽  
pp. 506 ◽  
Author(s):  
Abani K Patar ◽  
Surya Bhan ◽  
Donkupar Syiem ◽  
Anupama Sharma
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Diabetic Control ◽  
Protein Carbonyl ◽  
Control Group ◽  
Diabetic Mice ◽  
Ultrastructural Studies ◽  
Ameliorative Effect ◽  
Group A ◽  
Group B

The aim of this present study was to investigate the effect of chlorophyllin (CHL) on oxidative stress in Streptozotocine (STZ) induced diabetic mice. For the study, mice were divided into Group A: normal control, Group B: diabetic control, Group C: diabetic mice treated with the ascorbic acid, and Group D: diabetic mice treated with CHL. Levels of Reactive Oxygen Species (ROS), lipid peroxidation, protein carbonyl, superoxide dismutase (CuZn SOD &amp;Mn-SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR) activities were examined in kidney and heart tissues of different experimental groups. Histological and ultrastructuralstudies were also carried out to evaluate any changes in tissues as well as sub-cellular organelles. ROS, lipid peroxidation, and protein carbonyl levels have been significantly decreased with concomitant increased of CuZn SOD, Mn-SOD, CAT, GPx, and GR activity in CHLtreated diabetic mice. The histological and ultrastructural studies showed that CHL attenuates the detrimental effect of oxidative stress and alleviated tissue injuries in STZ induced diabetic mice. These results suggested that CHL possesses antioxidative activity and has the potential to amelioratediabetes-associated oxidative stress in mice.

scholarly journals Studies of the Biochemical Effects of Arsenic Content of Carbide Induced Ripe Banana Fruit in the Rat

2019 ◽  
Vol 35 (4) ◽  
pp. 1332-1337
Author(s):  
M. I Otite –Douglas ◽  
E. A Fadairo
Keyword(s):  
Lipid Peroxidation ◽  
Body Weight ◽  
Body Weight Gain ◽  
Weight Ratio ◽  
Calcium Carbide ◽  
Arsenic Content ◽  
Banana Fruit ◽  
High Concentration ◽  
Body Weight Ratio ◽  
Biochemical Indices

Arsenic is a well-known poison and it is found in trace amount in calcium carbide use for welding purposes and secondarily use by farmers and traders in Warri Metropolis to induce ripening processes in foods. This study was designed to evaluate the concentration of arsenic in selected banana fruits within Warri metropolis. It was also designed to determine its effects on some key biochemical indices of toxicity. The atomic absorption method was used to determine arsenic content of fruits and the biochemical indices evaluated were liver body weight ratio, body weight gain, the extent of lipid peroxidation in the liver organ and plasma, and the activities of alkaline phosphatases in the plasma and liver. Results showed a high concentration of arsenic in carbide-induced ripe banana (CTB) with an average value of 0.11mg/kg wet mass of test banana relative to the carbide-free banana (CFB) control with a value of <0.001 mg/kg. Our findings also showed a slight increase in body weight and decrease in liver body weight ratio of CTB rats, but the changes were not significant P>0.05 when compared to the control (CFB). However, there was a significant (P<0.05) decrease in body weight and increase in organ body weight ratios of arsenic-only exposed rats relative to the control. The activities of alkaline phosphatase in plasma increased significantly (P<0.05) for the groups of rats exposed to CTB and arsenic only via feed relative to their respective controls. The plasma and liver malondialdehyde (MDA) levels of rats exposed to CTB and arsenic only via feed were also elevated in this present study when compared to their respective controls however, the levels were not significant (P>0.05). This study shows the possibility of Plasma -ALP alteration and changes in levels of tissue lipid peroxidation products of carbide -treated ripe banana fruits. There is therefore the need for an urgent regulation on the use of carbide in the induction of ripening of fruits.

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