ABSTRACT
Selenium (Se) and zinc (Zn) are essential trace elements with antioxidant properties, and their supplementation has been shown to be protective against the toxicity of various environmental and dietary substances. The aim of this study was to investigate the potential protective effect of selenium and zinc as adjuvants against barium (Ba) toxicity in lactating rats and their offspring. The pregnant rats were divided into six groups: the first as control; group 2 received barium (67 ppm) in the drinking water; group 3 had combined Ba + Se (0.5 mg/kg) in the diet; group 4 received Zn (50 mg/kg bw) by gavage together with Ba; groups 5 and 6, positive controls, were treated with selenium (0.5 mg/kg) and zinc (50 mg/kg bw), respectively. MDA, H2O2, AOPP, CAT, GPx, and SOD levels were measured and lung histopathology was performed. Our results showed that barium administration caused lung damage as evidenced by an increase in MDA, H2O2, and AOPP levels and a decrease in the activities of CAT, GPx, and SOD in mothers and their offspring. A decrease in lung GSH, NPSH, and MT levels was also observed. Supplementation of Ba-treated rats with Se and/or Zn significantly improved the pulmonary antioxidant status of mothers and their offspring. Histopathological examinations were also consistent with the results of biochemical parameters, suggesting the beneficial role of Se and Zn supplementation, as evidenced by less accumulation of collagen fibers as studied by hematoxylin and eosin (H&E) and Masson's trichrome staining. In conclusion, we demonstrate the adverse effects of maternal barium exposure during pregnancy and on neonatal lung health and the protective effects of selenium and zinc in preventing the adverse effects of barium exposure.
Subject(s)
Barium Compounds , Lactation , Lung , Oxidative Stress , Selenium , Zinc , Animals , Selenium/pharmacology , Oxidative Stress/drug effects , Zinc/pharmacology , Female , Rats , Pregnancy , Lung/drug effects , Lung/pathology , Chlorides/toxicity , Antioxidants/pharmacology , Rats, WistarABSTRACT
The current study was conducted to assess the beneficial effect of selenium (Se) on maneb-induced cardiotoxicity and fatty acid alterations in adult mice. Swiss albino male mice were assigned into four experimental groups. The first group consisted of negative controls. The second group represented the positive controls where mice received daily, via the diet, sodium selenite at a dose of 0.2 mg/kg. For the third group, mice were subjected to intraperitoneal injections of maneb (30 mg/kg BW). The fourth group (MB+Se) received daily the same dose of maneb as group 3 along with sodium selenite at the same dose as group 2. Mice exposure to maneb caused cardiotoxicity as indicated by an increase in malondialdehyde, hydrogen peroxide, and protein carbonyl levels, and an alteration of the antioxidant defense system (catalase, glutathione peroxidase, superoxide dismutase, glutathione, and vitamin C). Plasma lactate dehydrogenase activity and total cholesterol, triglyceride, and low-density lipoprotein cholesterol levels increased, while high-density lipoprotein cholesterol level decreased. Results showed also a decrease in the amount of n-3 PUFA, docosahexaenoic, docosapentaenoic, and eicosapentaenoic acids. However, an increase in the levels of MUFA, cis-vaccenic, and palmitoleic acids was observed. Co-administration of Se restored the parameters indicated above to near control values. The histopathological findings confirmed the biochemical results. Selenium could be a useful and efficient agent against maneb-induced cardiotoxicity.
Subject(s)
Antioxidants , Cardiotoxicity , Maneb , Selenium , Animals , Antioxidants/pharmacology , Cholesterol , Lipid Peroxidation , Maneb/toxicity , Mice , Oxidative Stress , Selenium/pharmacology , Sodium Selenite , Superoxide Dismutase/metabolismABSTRACT
Hexavalent chromium (chromium (VI)), a highly toxic heavy metal, is a common pollutant of aquatic ecosystems. The present study aimed to elucidate the potential toxic effects of chromium (VI) on oxidative stress biomarkers and fatty acids profile in the gills and digestive gland of Venus verrucosa, an ecologically and economically important bivalve species. Three doses of chromium (VI) (1, 10 and 100 µg.L-1) were chosen for V. verrucosa exposure during 7 days under controlled conditions. A significant increase in the levels of malondialdehyde, lipid hydroperoxides and hydrogen peroxide was observed in the gills and digestive gland of chromium (VI)-exposed V. verrucosa as compared to the control group. Furthermore, an induction of enzymatic antioxidant activities (superoxide dismutase, glutathione peroxidase and glutathione S-transferase) and an enhancement of non-enzymatic antioxidant levels (non-protein thiols, glutathione and vitamin C) were marked. An alteration of fatty acids composition was also noted following chromium (VI) exposure. The obtained results highlighted the importance of assessing oxidative damage biomarkers and fatty acids profile in the study of chromium (VI)-induced toxicity in V. verrucosa.
Subject(s)
Antioxidants/metabolism , Bivalvia/drug effects , Chromium/toxicity , Fatty Acids/metabolism , Oxidative Stress/drug effects , Water Pollutants, Chemical/toxicity , Animals , Biomarkers/metabolism , Bivalvia/metabolism , Ecosystem , Gills/drug effects , Gills/metabolism , Glutathione/metabolism , Glutathione Peroxidase/metabolism , Glutathione Transferase/metabolism , Malondialdehyde/metabolism , Superoxide Dismutase/metabolismABSTRACT
Zinc is one of the important essential trace minerals to human health due to its antioxidant properties. The present study was conducted to elucidate its potential protective role against maneb-induced nephrotoxicity. For this purpose, animals were randomly divided into four groups of six each. Mice of group I (negative controls) have received daily 0.5 ml of distilled water, a solvent of maneb. Mice of group II (MB) have received 30 mg/kg bw of maneb daily by intraperitoneal way. Mice of group III (MB + Zn) have received the same dose of maneb as group II, along with ZnSO4 (30 mg/kg bw) daily. Mice of group IV (Zn), considered as positive controls, have received the same dose of ZnSO4 as group III daily. Our results revealed that ZnSO4 co-administration to maneb-treated mice decreased kidney levels of malondialdehyde, hydrogen peroxide, protein carbonyls, and advanced oxidation protein products; the levels of non-enzymatic antioxidants like vitamin C, glutathione, and metallothionein. It recovered the alteration of antioxidant enzyme activities (catalase, superoxide dismutase, and glutathione peroxidase) and attenuated DNA fragmentation. Furthermore, this essential trace element was also able to alleviate kidney biomarkers' alterations by lowering plasma levels of creatinine, urea, uric acid, and lactate dehydrogenase. In addition, the histopathological changes induced by maneb were improved following zinc administration. Our results indicated that zinc might be beneficial against maneb-induced renal oxidative damage in mice.
Subject(s)
Glutathione Peroxidase , Glutathione , Kidney , Maneb , Superoxide Dismutase , Zinc , Animals , Mice , Antioxidants , DNA Damage , Glutathione/chemistry , Glutathione Peroxidase/chemistry , Glutathione Peroxidase/metabolism , Kidney/physiopathology , Oxidative Stress , Random Allocation , Superoxide Dismutase/chemistry , Zinc/chemistryABSTRACT
The present work evaluated the possible protective effects of quercetin against glyphosate-induced hepatotoxicity in adult rats. Rats were randomly divided into three groups: a control group (C), a glyphosate-treated group (Gly) and a group treated with both glyphosate and quercetin (Gly+QE). During the experimental period (15 days), glyphosate (50 mg/kg b.w.) was administered every two days by intraperitoneal way while quercetin (20 mg/kg b.w./day) was administered daily by gavage. Glyphosate-induced hepatic oxidative stress was evidenced by the increased levels of malondialdehyde, hydrogen peroxide, advanced oxidation protein products and protein carbonyls with a significant decrease in enzymatic (superoxide dismutase, catalase, glutathione peroxidase) and non-enzymatic (non-protein thiols, glutathione, vitamin C) antioxidants. Plasma biomarkers of hepatotoxicity (AST, ALT, ALP, γ-GT, albumin) were also altered. Moreover, glyphosate induced DNA damage, up-regulated metallothionein (MT I and MT II) genes expression and provoked histopathological changes in rats' liver. Quercetin supplementation to glyphosate-treated rats markedly ameliorated all the parameters indicated above as well as the liver histoarchitecture. Therefore, quercetin might have beneficial effects against glyphosate-induced hepatotoxicity in rats.
Subject(s)
Glycine/analogs & derivatives , Metallothionein , Quercetin , Animals , Antioxidants , Glycine/physiology , Liver , Metallothionein/drug effects , Metallothionein/metabolism , Oxidation-Reduction , Oxidative Stress , Quercetin/pharmacology , Random Allocation , Rats , Rats, Wistar , Superoxide Dismutase , GlyphosateABSTRACT
The present study pertains to the possible adverse effects of penconazole exposure on the lung of adult rats, and to the potential ability of vitamin E (Vit E) in mitigating the toxicity induced by this fungicide. Male Wistar rats were divided into four groups of six animals each: Group I (Controls): rats drank distilled water; Group II (PEN): rats received, by gavage, 50â¯mg/kg body weight (1/40 LD50) of penconazole every 2 days during 10 days; Group III (Vit E): rats received daily 100â¯mg α-tocopherol acetate/kg body weight during 10 days by gavage; and Group IV (Vit Eâ¯+â¯PEN): rats received both vitamin E (100â¯mg α-tocopherol acetate/kg body weight) and penconazole (50â¯mg/kg body weight), being vitamin E given as a daily dosage and penconazole every 2 days, by gavage during 10 days. Results showed that penconazole induced oxidative stress in the lung demonstrated by an increase in malondialdehyde (+77%), hydrogen peroxide (+58%) and advanced oxidation protein product (+22%) levels, as compared to the controls. Furthermore, a decrease in the activities of catalase (-41%), superoxide dismutase (-45%), glutathione peroxidase (-23%) and acetylcholinesterase (-67%), and an increase in the levels of non-protein thiols (+17%), glutathione (+7%) and vitamin C (+44%) were registered. Abnormalities in lung histological sections such as alveolar edema, infiltration of inflammatory cells (leukocytes) and emphysema, were also observed following penconazole exposure. Vitamin E ameliorated the biochemical parameters, as well as the histological impairments induced by this fungicide. In conclusion, our study demonstrated that vitamin E, a natural antioxidant, was effective in alleviating penconazole-induced lung damage in Wistar rats.
Subject(s)
Cholinergic Agents/adverse effects , Lung/pathology , Triazoles/adverse effects , Vitamin E/pharmacology , Acetylcholinesterase/metabolism , Animals , Antioxidants/metabolism , Body Weight/drug effects , Hydrogen Peroxide/metabolism , Lipid Peroxidation/drug effects , Lung/drug effects , Lung Injury/pathology , Male , Malondialdehyde/metabolism , Organ Size/drug effects , Oxidation-Reduction/drug effects , Rats, Wistar , Vitamin E/therapeutic useABSTRACT
CONTEXT: Barium (Ba) may induce oxidative stress leading to tissues injury. OBJECTIVE: Our study investigated the therapeutic efficiency of zinc (Zn) and selenium (Se) against neurotoxicity induced by Ba in adult rats and their progeny. MATERIAL AND METHODS: Pregnant rats are exposed either to Ba (67 ppm), Ba + Zn, Ba + S or to only Zn and Se. RESULTS: In Ba-treated rats, there was an increase of MDA, H2O2, AOPP levels and SOD activity in the cerebellum of dams and their pups, a decrease in GPx, CAT, AChE, Na+K+-ATPase and Mg2+-ATPase activities, GSH and NPSH levels. These changes were confirmed by histological damages. Co-administration of Zn or Se to Ba-treated rats ameliorated the biochemical and histological aspects. CONCLUSION: Our results revealed that Zn and Se have shown promising effects against Ba toxicity in the cerebellum of adult rats and their suckling pups.
Subject(s)
Adenosine Triphosphatases/metabolism , Barium/adverse effects , Cell Membrane/metabolism , Cerebellum/drug effects , Oxidative Stress/drug effects , Selenium/pharmacology , Zinc/pharmacology , Acetylcholinesterase/metabolism , Animals , Cell Membrane/drug effects , Cerebellum/cytology , Cerebellum/metabolism , Dose-Response Relationship, Drug , Female , Glutathione/metabolism , Hydrogen Peroxide/metabolism , Lipid Peroxidation/drug effects , Pregnancy , Rats , Rats, WistarABSTRACT
Data on the individual nephrotoxic effects of imidacloprid (IMI) and gibberellic acid (GA3) are scarce. Moreover, there is a lack of information about their combined effects on the renal tissue. Our study investigated the effects of IMI and GA3 separately or together on rats kidney. IMI (64 mg/kg bw) was given for 3 weeks by gavage either individually or in combination with GA3 (200 mg/L) via drinking water. IMI associated or no with GA3 increased the levels of kidney malondialdehyde, advanced oxidation protein products, protein carbonyls and metallothionein, plasma creatinine, urea, blood urea nitrogen and lactate dehydrogenase activity. A decline of kidney uric acid level and antioxidant status was also observed. All these changes were supported by histopathological observations. Our results highlighted the role of IMI and/or GA3-induced nephrotoxicity. Co-exposure to IMI and GA3 exhibited synergism in biochemical kidney variables and histopathology and antagonism in physical and morphological parameters.
Subject(s)
Gibberellins/toxicity , Insecticides/toxicity , Kidney/drug effects , Neonicotinoids/toxicity , Nitro Compounds/toxicity , Plant Growth Regulators/toxicity , Poisoning/physiopathology , Renal Insufficiency/etiology , Administration, Oral , Animals , Biomarkers/blood , Biomarkers/metabolism , Blood Urea Nitrogen , Drug Interactions , Gibberellins/administration & dosage , Insecticides/administration & dosage , Kidney/metabolism , Kidney/pathology , Kidney/physiopathology , Lipid Peroxidation/drug effects , Metallothionein/metabolism , Neonicotinoids/administration & dosage , Nitro Compounds/administration & dosage , Organ Size/drug effects , Oxidation-Reduction , Oxidative Stress/drug effects , Oxidoreductases/metabolism , Poisoning/etiology , Protein Carbonylation/drug effects , Random Allocation , Rats, Wistar , Renal Insufficiency/metabolism , Renal Insufficiency/pathology , Renal Insufficiency/physiopathology , Weight Gain/drug effectsABSTRACT
High-cholesterol diet (HCD) is suspected to produce in excess free radicals having adverse effects on human health and causing atherosclerosis damage in heart tissues. In our study, the effects of zebra blenny protein hydrolysates (ZBPHs) were investigated on cardiac oxidant/antioxidant status as well as DNA damage and histopathological disorders in rats, fed with a hypercholesterolemic diet. The molecular weight distribution of the hydrolysates was determined by size exclusion chromatography, which analyzed a representative hydrolysate type with a weight range of 3-20kDa. ZBPHs effectively protected heart genomic DNA against oxidative damage induced by Fenton's reagent. HCD promoted oxidative stress with a rise in serum aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) activities and thiobarbituric acid reactive substance (TBARS), advanced oxidation protein product (AOPP) and hydrogen peroxide (H2O2) levels in heart tissues. An increase in glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) activities as well as a fall in ATPase activities and glutathione (GSH) level was also noted in heart of hypercholesterolemic rats. Treatment with ZBPHs ameliorated the biochemical parameters cited above. In addition, pre-treatment with ZBPHs prevented DNA fragmentation. The histopathological findings confirmed the biochemical results and the potential antioxidant activities of ZBPHs which can help the cure and management of cardiovascular diseases induced by high-cholesterol levels.
Subject(s)
Cholesterol, Dietary , DNA Damage/drug effects , Diet, High-Fat/adverse effects , Fish Proteins , Heart/drug effects , Oxidative Stress/drug effects , Animals , Cholesterol, Dietary/administration & dosage , Cholesterol, Dietary/adverse effects , Fish Proteins/chemistry , Fish Proteins/pharmacology , Fishes , Male , Peptides/chemistry , Peptides/pharmacology , Protein Hydrolysates/chemistry , Protein Hydrolysates/pharmacology , Rats , Rats, WistarABSTRACT
Nowadays, liver diseases constitute a major health problem in the world. The objective of the present study was to elucidate the hepatotoxicity induced by barium chloride (BaCl2) administered at graded doses in order to evaluate redox state and membrane-bound ATPases in the liver of adult rats. Our results showed, after 21 days of treatment with barium at doses 67 150 and 300 ppm, an increase in hepatic biomarkers such as AST, ALT and GGT activities and in bilirubin and albumin levels. A significant increase in MDA, LOOHs, H2O2, AOPP and PCO levels in liver of treated rats with graded doses of BaCl2 was also observed suggesting the implication of oxidative stress with a significant relation between dose and response. Moreover, LDH activity increased in plasma and decreased in liver of all treated groups. Antioxidant activities of glutathione peroxidase and catalase decreased, especially with the highest dose of barium, indicating a failure of antioxidant system defense. Additionally, the activities of Na+K+-ATPase and Mg2+-ATPase significantly decreased in all treated groups. Our biochemical findings were supported by histological observations. These results highlight the subchronic hepatotoxicity of barium.
Subject(s)
Adenosine Triphosphatases/metabolism , Barium Compounds/toxicity , Chlorides/toxicity , Liver/drug effects , Membrane Proteins/metabolism , Animals , Barium Compounds/administration & dosage , Chlorides/administration & dosage , Dose-Response Relationship, Drug , Female , Hydrogen Peroxide/metabolism , L-Lactate Dehydrogenase/metabolism , Lipid Peroxidation , Liver/enzymology , Liver/metabolism , Liver/pathology , Liver Function Tests , Metallothionein/metabolism , Oxidation-Reduction , Rats , Rats, WistarABSTRACT
The present study investigates the toxic effects of acrylamide (ACR) administered to rats at two doses on (i) oxidative stress and disruption of pro-oxidant/antioxidant balance in hepatic cells and (ii) its correlation with metallothioneins (MTs) genes expression, DNA damage and histomorphological changes. Treated rats with 20 and 40 mg/kg body weight of ACR led to an increase in malondialdehyde, hydrogen peroxide, advanced oxidation protein products, protein carbonyl levels as well as an alteration in the antioxidant status. Total MT content in the liver and MT I and MT II genes induction were increased. Plasma transaminases activities, albumin, total protein and glucose levels were also increased, while alkaline phosphatase activity was decreased. Moreover, total cholesterol (TC), triglyceride, low-density lipoprotein cholesterol (LDL-C) levels, TC/high-density lipoprotein cholesterol (HDL-C) and LDL-C/HDL-C ratios were increased, while HDL-C decreased in a dose-dependent manner. A random DNA degradation was observed only in the liver of ACR-treated rats with the highest dose. These changes were confirmed by histopathological observations.
Subject(s)
Acrylamide/toxicity , DNA Fragmentation/drug effects , Liver/drug effects , Metallothionein/metabolism , Alanine Transaminase/blood , Alkaline Phosphatase , Animals , Aspartate Aminotransferases/blood , Biomarkers/blood , Cholesterol/blood , DNA Damage/drug effects , Dose-Response Relationship, Drug , Female , Lipid Peroxidation/drug effects , Liver/pathology , Malondialdehyde/blood , Metallothionein/genetics , Oxidative Stress/drug effects , Rats , Rats, Wistar , Reactive Oxygen Species/metabolism , Serum Albumin/metabolism , Triglycerides/bloodABSTRACT
CONTEXT: Nitraria retusa (Forssk.) Asch. (Nitrariaceae) is a medicinal plant which produces edible fruits whose antioxidant activity has been demonstrated. OBJECTIVE: The current study elucidates the potential protective effect of N. retusa fruit aqueous extract against nephrotoxicity induced by penconazole, a triazole fungicide, in the kidney of adult rats. MATERIALS AND METHODS: Adult Wistar rats were exposed either to penconazole (67 mg/kg body weight), or to N. retusa extract (300 mg/kg body weight) or to their combination. Penconazole was administered by intra-peritoneal injection every 2 days from day 7 until day 15, the sacrifice day, while N. retusa extract was administered daily by gavage during 15 days. Oxidative stress parameters, kidney biomarkers and histopathological examination were determined. RESULTS: Nitraria retusa extract administration to penconazole treated rats decreased kidney levels of malondialdehyde (-10%), hydrogen peroxide (-12%), protein carbonyls (PCOs, -11%) and advanced oxidation protein products (AOPP, -16%); antioxidant enzyme activities: catalase (-13%), superoxide dismutase (-8%) and glutathione peroxidase (GPx, -14%), and the levels of non-enzymatic antioxidants: non-protein thiols (-9%), glutathione (-7%) and metallothionein (-12%). Furthermore, this plant extract prevented kidney biomarker changes by reducing plasma levels of creatinine, urea, uric acid and LDH and increasing those of ALP and GGT. Histopathological alterations induced by penconazole (glomeruli fragmentation, Bowman's space enlargement, tubular epithelial cells necrosis and infiltration of inflammatory leucocytes) were attenuated following N. retusa administration. DISCUSSION AND CONCLUSION: Our results indicated that N. retusa fruit extract had protective effects against penconazole-induced kidney injury, which could be attributed to its phenolic compounds.
Subject(s)
Kidney/drug effects , Magnoliopsida , Oxidative Stress/drug effects , Plant Extracts/pharmacology , Triazoles/toxicity , Animals , Fruit/chemistry , Kidney/metabolism , Kidney/pathology , Lipid Peroxidation/drug effects , MAP Kinase Signaling System/drug effects , Male , NF-kappa B/physiology , Polyphenols/analysis , Rats , Rats, WistarABSTRACT
Acrylamide (ACR) is one of the most important contaminants occurring in foods heated at high temperatures. The aim of this study is to investigate the protective efficacy of extra virgin olive oil (EVOO), a main component of the Mediterranean diet, against nephrotoxicity induced by ACR. Rats have received by gavage during 21 days either ACR (40 mg/kg body weight) or ACR-associated with EVOO (300 µl) or only EVOO (300 µl). Acrylamide induced nephrotoxicity as evidenced by an increase in malondialdehyde (MDA), hydrogen peroxide (H2O2), protein carbonyls (PCOs) and a decrease in glutathione, non-protein thiols (NPSHs), and vitamin C levels. Activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) were also decreased. Lactate dehydrogenase (LDH) activity, creatinine, urea, and uric acid, urinary volume and creatinine clearance levels were modified. EVOO supplementation improved all the parameters indicated above. Kidney histoarchitecture confirmed the biochemical parameters and the beneficial role of EVOO. EVOO, when added to the diet, may have a beneficial role against kidney injury by scavenging free radicals and by its potent antioxidant power.
Subject(s)
Acrylamide/toxicity , Antioxidants/pharmacology , Kidney Diseases/prevention & control , Olive Oil/pharmacology , Oxidative Stress/drug effects , Animals , Catalase/metabolism , Dietary Supplements , Female , Glutathione/metabolism , Glutathione Peroxidase/metabolism , Hydrogen Peroxide/metabolism , Kidney/physiopathology , L-Lactate Dehydrogenase/blood , Malondialdehyde/metabolism , Random Allocation , Rats , Rats, Wistar , Superoxide Dismutase/metabolismABSTRACT
Ethanol consumption-induced oxidative stress that is a major etiological factor has been proven to play important roles in organs' injury. In the present study, we investigated the protective effect of fish protein hydrolysate prepared from the heads and viscera of sardinelle (Sardinella aurita) (SPH) against the toxicity of ethanol on the liver and kidney of adult male rats. Animals were divided into four groups of six animals each: group C served as control, group Eth received 30 % ethanol solution at the dose of 3 g/kg body weight, group SPH received only 7.27 mg of SPH/kg body weight, and group Eth-SPH received ethanol and SPH simultaneously at the doses of 30 % and 7.27 mg/kg body weight, respectively. All groups were treated by gavage way for 15 days. Ethanol treatment decreased the defense enzymatic system including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), which increased after the co-administration of SPH. Malondialdehyde (MDA) and toxicity biomarker levels such as aspartate transaminase (AST) and alanine transaminase (ALT) and alcaline phosphatase (ALP) and gamma-glutamyl transaminase (GGT) activities were enhanced after chronic ethanol treatment and reduced by co-treatment with SPH. The histological examination of the liver and kidney confirmed biochemical changes in ethanol-treated rats and demonstrated the protective role of SPH.
Subject(s)
Ethanol/antagonists & inhibitors , Fish Proteins/pharmacology , Kidney/drug effects , Liver/drug effects , Oxidative Stress/drug effects , Protective Agents/pharmacology , Protein Hydrolysates/pharmacology , Alanine Transaminase/metabolism , Animals , Aspartate Aminotransferases/metabolism , Body Weight/drug effects , Catalase/metabolism , Ethanol/pharmacology , Fishes , Glutathione Peroxidase/metabolism , Male , Malondialdehyde/pharmacology , Rats , Rats, Wistar , Superoxide Dismutase/metabolismABSTRACT
Our study pertains to the potential ability of selenium, used as a nutritional supplement, to alleviate oxidative stress induced by aluminum chloride in the lung tissue. Rats have received during 21 days either aluminum chloride (AlCl3) (400 ppm) via drinking water, AlCl3 associated with Na2SeO3 (0.5 mg/kg of diet), or only Na2SeO3. Exposure of rats to AlCl3 induced lung oxidative stress with an increase of malondialdehyde, hydrogen peroxide, and protein carbonyls levels. An alteration of lactate dehydrogenase activities and antioxidant redox status, enzymatic (catalase, superoxide dismutase, and glutathione peroxidase), and non-enzymatic (non-protein thiols, glutathione, metallothionein, and vitamin C) was also observed. These biochemical modifications were substantiated by histopathological data showing alveolar edema, a large number of hemosiderin-laden macrophages, and emphysema. Se supplementation attenuated the levels of oxidative stress by restoring antioxidant state and improved lung histological damage. Our results revealed that Se, a trace element with antioxidant properties, was effective in preventing lung damage.
Subject(s)
Aluminum Compounds/toxicity , Chlorides/toxicity , Lung/drug effects , Oxidative Stress/drug effects , Selenium/pharmacology , Aluminum Chloride , Animals , Antioxidants/metabolism , Antioxidants/pharmacology , Ascorbic Acid/metabolism , Body Weight/drug effects , Catalase/metabolism , Drinking/drug effects , Eating/drug effects , Female , Glutathione/metabolism , Glutathione Peroxidase/metabolism , Hydrogen Peroxide/metabolism , L-Lactate Dehydrogenase/metabolism , Lung/metabolism , Lung/pathology , Malondialdehyde/metabolism , Metallothionein/metabolism , Organ Size/drug effects , Oxidation-Reduction/drug effects , Protein Carbonylation/drug effects , Rats, Wistar , Superoxide Dismutase/metabolismABSTRACT
Several metals including barium (Ba) known as environmental pollutants provoke deleterious effects on human health. The present work pertains to the potential ability of selenium (Se) and/or vitamin C, used as nutritional supplements, to alleviate the toxic effects induced by barium chloride (BaCl2) in the heart of adult rats. Animals were randomly divided into seven groups of six each: group 1, serving as negative controls, received distilled water; group 2 received in their drinking water BaCl2 (67 ppm); group 3 received both Ba and Se (sodium selenite 0.5 mg kg-1 of diet); group 4 received both Ba and vitamin C (200 mg kg-1 bodyweight) via force feeding; group 5 received Ba, Se, and vitamin C; and groups 6 and 7, serving as positive controls, received either Se or vitamin C for 21 days. The exposure of rats to BaCl2 caused cardiotoxicity as monitored by an increase in malondialdehyde, hydrogen peroxide, and advanced oxidation protein product levels, a decrease in Na+-K+ adenosine triphosphatase (ATPase), Mg2+ ATPase, and acetylcholinesterase activities and in antioxidant defense system (catalase, glutathione peroxidase, superoxide dismutase, glutathione, and nonprotein thiols). Plasma lactate dehydrogenase and creatine kinase activities, total cholesterol, triglyceride, and low-density lipoprotein-cholesterol levels increased, while high-density lipoprotein-cholesterol level decreased. Coadministration of Se and/or vitamin C restored the parameters indicated above to near control values. The histopathological findings confirmed the biochemical results. Se and vitamin C may be a promising therapeutic strategy for Ba-induced heart injury.
Subject(s)
Ascorbic Acid/pharmacology , Barium Compounds/toxicity , Chlorides/toxicity , Heart Diseases/chemically induced , Selenium/pharmacology , Acetylcholinesterase/metabolism , Adenosine Triphosphatases/metabolism , Animals , Ascorbic Acid/administration & dosage , Diet , Gene Expression Regulation, Enzymologic/drug effects , Heart/drug effects , Heart Diseases/drug therapy , Hydrogen Peroxide , Lipid Peroxidation , Myocardium/enzymology , Myocardium/pathology , Organ Size/drug effects , Rats , Rats, Wistar , Selenium/administration & dosage , Sodium-Potassium-Exchanging ATPase/metabolismABSTRACT
Aluminum chloride (AlCl3) and acrylamide (ACR) are well known as environmental pollutants inducing oxidative stress. Our study investigated the effects of these contaminants and if the hydrophilic fraction of extra virgin olive oil was able to prevent lung oxidative stress and DNA damage. Animals were divided into four groups of six each: group 1, serving as controls, received distilled water; group 2 received in drinking water aluminum chloride (50 mg/ kg body weight) and by gavage acrylamide (20 mg/kg body weight); group 3 received both aluminum and acrylamide in the same way and the same dose as group 2 and hydrophilic fraction from olive oil (OOHF) (1 ml) by gavage; group 4 received only OOHF by gavage. Exposure of rats to both aluminum and acrylamide provoked oxidative stress in lung tissue based on biochemical parameters and histopathological alterations. In fact, we have observed an increase in malondialdehyde (MDA), H2O2, and advanced oxidation protein product (AOPP) and a decrease in reduced glutathione (GSH), non-protein thiols (NPSH), and vitamin C levels. Activities of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) were also decreased. Histopathological changes in lung tissue were noted like emphysema, vascular congestion, and infiltration of inflammatory cells. A random DNA degradation was observed on agarose gel in the lung of AlCl3 and acrylamide (ACR)-treated rats. Co-administration of OOHF to treated rats improved biochemical parameters to near control values and lung histoarchitecture. The smear formation of genomic DNA was reduced. The hydrophilic fraction of extra virgin olive oil might provide a basis for developing a new dietary supplementation strategy in order to prevent lung tissue damage.
Subject(s)
Acrylamide/toxicity , Aluminum/toxicity , DNA Damage/drug effects , Lung Injury/prevention & control , Olive Oil , Aluminum Chloride , Aluminum Compounds , Animals , Antioxidants/metabolism , Chlorides , Diet , Dietary Supplements , Glutathione/metabolism , Glutathione Peroxidase/metabolism , Hydrogen Peroxide/pharmacology , Male , Malondialdehyde/metabolism , Oxidation-Reduction , Oxidative Stress/drug effects , Rats , Rats, Wistar , Superoxide Dismutase/metabolismABSTRACT
Hepatotoxicity, induced by aluminium chloride (AlCl3), has been well studied but there are no reports about liver metallothionein (MT) genes induction. Therefore, it is of interest to establish the mechanism involving the relation between MT gene expression levels and the oxidative stress status in hepatic cells of aluminium-treated rats. Aluminium (Al) was administered to rats in their drinking water at a dose of 50 mg/kg body weight for three weeks. AlCl3 provoked hepatotoxicity objectified by an increase in malondialdehyde (MDA), hydrogen peroxide (H2O2), advanced oxidation protein products (AOPP), protein carbonyls (PCO) and a decrease in reduced glutathione (GSH), non-protein thiols (NPSH) and vitamin C. CAT and Glutathione peroxidase (GPx) activities were decreased while Mn-SOD gene expression, total Metallothionein content and MT I and MT II genes induction were increased. There are changes in plasma of some trace elements, albumin levels, transaminases, LDH and ALP activities. All these changes were supported by histopathological observations.
Subject(s)
Aluminum/toxicity , Gene Expression Regulation/drug effects , Liver/metabolism , Metallothionein/metabolism , Oxidative Stress/drug effects , Animals , Blotting, Western , Enzyme-Linked Immunosorbent Assay , Liver/drug effects , Liver/pathology , Male , Metallothionein/genetics , RNA, Messenger/genetics , Rats , Rats, Wistar , Real-Time Polymerase Chain Reaction , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
Accumulation of aluminium and acrylamide in food is a major source of human exposure. Their adverse effects are well documented, but there is no information about the health problems arising from their combined exposure. The aim of the present study was to examine the possible neurotoxic effects after co-exposure of pregnant and lactating rats to aluminium and acrylamide in order to evaluate redox state, cholinergic function and membrane-bound ATPases in the cerebellum of adult rats and their progeny. Pregnant female rats have received aluminium (50 mg/kg body weight) via drinking water and acrylamide (20 mg/kg body weight) by gavage, either individually or in combination from the 14th day of pregnancy until day 14 after delivery. Exposure to these toxicants provoked an increase in malondialdehyde (MDA) and advanced oxidation protein product (AOPP) levels and a decrease in SOD, CAT, GPx, Na+K+-ATPase, Mg2+-ATPase and AChE activities in the cerebellum of mothers and their suckling pups. A reduction in GSH, NPSH and vitamin C levels was also observed. These changes were confirmed by histological results. Interestingly, co-exposure to these toxicants exhibited synergism based on physical and biochemical variables in the cerebellum of mothers and their progeny.
Subject(s)
Acetylcholine/metabolism , Acrylamide/toxicity , Aluminum/toxicity , Cerebellum/metabolism , Maternal Exposure/adverse effects , Prenatal Exposure Delayed Effects/metabolism , Advanced Oxidation Protein Products/metabolism , Animals , Female , Humans , Male , Malondialdehyde/metabolism , Oxidation-Reduction/drug effects , Oxidoreductases/metabolism , Pregnancy , Prenatal Exposure Delayed Effects/chemically induced , RatsABSTRACT
CONTEXT: Pomegranate peel (PP) has health benefits including antibacterial, antioxidant, anti-inflammatory, and antimutagenic properties. OBJECTIVE: This study investigated the biochemical composition and protective effects of PP against hematotoxicity and genotoxicity induced by barium chloride (BaCl2) in adult rats. MATERIALS AND METHODS: Adult Wistar rats were divided into four groups of six each: control, barium (67 ppm via drinking water), PP (5% via diet), and their combination during 21 d. Oxidative stress was determined by MDA, AOPP, and antioxidant status: CAT, GPx, GSH, Vit C. Osmotic fragility (OF), chromosomal aberrations (CAs), and micronucleus (MN) assays were also studied. RESULTS: PP showed a rich composition of antioxidant compounds. DPPH test found IC50 value= 5.3 µg/mL and a high polysaccharides content (315 ± 5 mg/g of extract). In vivo study showed a decrease in red blood cells (70%) and platelet counts (46%), hemoglobin content (8%), hematocrit percent (7%), and an 80% increase of white blood cells in Ba-treated rats. A reduction in antioxidant status: catalase, glutathione peroxidase activities, glutathione, and vitamin C levels by 31, 21, 28, and 29%, respectively, and an increase in MDA (46%) and AOPP levels (72%) were also observed compared with controls. BaCl2-treatment showed a significant increase in the frequencies of total chromosomal aberrations with abnormal metaphases and micronucleus in bone-marrow cells. Oxidative stress induced by BaCl2 might be the major cause for chromosomal abnormalities leading to DNA damage. DISCUSSION AND CONCLUSION: A decrease in hematotoxic and genotoxic effects induced by PP is due to its powerful antioxidant capacity.