Membrane-bound ATPase Activity Research Articles

Acarbose Mitigates Age-Dependent Alterations in Erythrocyte Membrane Transporters During Aging in Rats.

Acarbose (ACA), a well-studied and effective inhibitor of α-amylase and α-glucosidase, is a postprandial-acting antidiabetic medicine. The membrane of the erythrocyte is an excellent tool for analyzing different physiological and biochemical activities since it experiences a range of metabolic alterations throughout aging. It is uncertain if ACA modulates erythrocyte membrane activities in an age-dependent manner. As a result, the current study was conducted to explore the influence of ACA on age-dependent deteriorated functions of transporters/exchangers, disrupted levels of various biomarkers such as lipid hydroperoxides (LHs), protein carbonyl (PCO), sialic acid (SA), total thiol (-SH), and erythrocyte membrane osmotic fragility. In addition to a concurrent increase in Na+/H+ exchanger activity and concentration of LH, PCO, and osmotic fragility, we also detected a considerable decrease in membrane-linked activities of Ca2+-ATPase (PMCA) and Na+/K+-ATPase (NKA), as well as concentrations of SA and -SH in old-aged rats. The aging-induced impairment of the activities of membrane-bound ATPases and the changed levels of redox biomarkers were shown to be effectively restored by ACA treatment.

VANILLIC ACID INHIBITS LUNG CARCINOGENESIS BY MODULATES GLYCOPROTEIN ABNORMALITIES, MEMBRANE-BOUND ENZYMES, AND INFLAMMATORY MARKERS

Objective: The current plan was accompanied to explicate the possible protective role of vanillic acid (VA), on modification in lipid peroxidation, inflammatory cytokines, membrane-bound enzymes, and glycoconjugates during B(a)P induced lung cancer in Swiss albino mice.
 Methods: Benzo(a)pyrene was administered orally (50 mg/kg b. wt) to induce lung cancer in Swiss albino mice. lipid peroxidation, serum marker enzymes, inflammatory cytokines, membrane-bound ATPases and protein-bound carbohydrate components (Hexose, hexosamine, sialic acid and fucose) and Mast cells and PAS staining were carried out.
 Results: Lung cancer possessing animals exhibited increased levels of lipid peroxidation, ADA, AHH, γ-GT, 5’-NT, LDH, cytokines such as TNF-α and IL-1β, protein-bound carbohydrate components (protein-hexose, hexosamine, sialic acid, and fucose) also diminished activity of membrane-bound ATPases (Na+/K+ATPases, Ca2+ATPases, and Mg2+ATPase). Treatment with VA significantly ameliorated all these activities.
 Conclusion: Overall, the present study evidence to the VA has effective anti-inflammatory in addition to free radical scavenging activity for the duration of lung carcinogenesis in Swiss albino mice.

AMELIORATION OF ACETAMINOPHEN-INDUCED HEPATOTOXICITY USING SOLANUM TORVUM SW. FRUIT EXTRACT IN WISTAR RATS

Objective: Ayurveda and Chinese pharmacopeia have highlighted the traditional medicinal uses of Solanum torvum Sw. The fruits are ethnomedical used in the treatment of liver and spleen enlargement, cough, and also used as a hematopoietic, antimicrobial, and analgesic agent. In the present study, the amelioration of acetaminophen (APAP)-induced hepatotoxicity of the aqueous extract of S. torvum Sw. fruits is evaluated.
 Methods: The hepatoprotective activity of the fruit extract against APAP insult was evaluated by assessing it is in vivo antioxidants status, membrane-bound adenosine triphosphatases (ATPases), and tricarboxylic acid (TCA) cycle marker enzymes and also through histopathological studies of the liver.
 Results: Administration of the aqueous fruit extract of the plant caused a significant increase in the in vivo antioxidant status as evident from the reduction in lipid peroxidation caused by APAP and improvement in the mitochondrial membrane stability which is proved from the activity of membrane-bound ATPases and TCA cycle marker enzymes. Histological studies also supported the fact that the plant extract proved to revive the architecture of the toxin damaged liver tissues in par with silymarin. The chemical pathological changes were consistent with histopathological observations suggesting marked hepatoprotective effect of the aqueous extract of S. torvum.
 Conclusion: The results showed that the extract of S. torvum Sw. fruits has hepatoprotective potential which may be due to the antioxidant activity of its phytoconstituents, especially flavonoids, alkaloids, phenolics, etc.

Repeated bifenthrin exposure alters hippocampal Nurr-1/AChE and induces depression-like behavior in adult rats

Exposure to insecticides has been associated with depression-like symptoms, especially among occupationally exposed populations, such as farmers. Although the neurotoxicity of pyrethroids such as bifenthrin (BF) is well established, it is still unclear whether exposure to BF may have deleterious effects on the hippocampus and thus behavior. We verified the hypothesis that repeated exposure to BF in a rat model elicits neurochemical and behavioral alterations, the latter of which reflects depression-related symptoms. Adult male Wistar rats (n = 12 per group) were orally administered with different doses of BF (0.6 or 2.1 mg/kg body weight (b.w.)) on a daily basis for 60 days; control rats received the vehicle (corn oil). Different biochemical changes were assessed in the hippocampus, a region of the brain regulating spatial memory; behavioral tests were also conducted. Our results revealed depressive-like behaviors that were expressed by increased despair behavior in the Forced-swimming test. Repeated exposure to BF also decreased acetylcholinesterase (AChE) activity in the hippocampus and butyrylcholinesterase (BuChE) activity in plasma. A significant reduction in the activities of hippocampal membrane-bound ATPases (Na+/K+-ATPase and Mg2+-ATPase) was also observed in BF-treated rats compared to controls. Furthermore, a significant decrease in mRNA expression and protein synthesis of both AChE and orphan nuclear receptor (Nurr-1), as well as in the expression of muscarinic–cholinergic receptor (M1 mAchR) and nicotinic–cholinergic receptor (nAchR2α) was observed in the hippocampus of treated rats compared to controls. Also, BF exposure induced apoptosis as assessed by hippocampal Casp-3 protein levels. Our findings suggest that repeated exposure to BF affects hippocampal signaling and Nurr-1/AChE, and this was accompanied by depression-like state in adult rats.

Rapamycin mitigates erythrocyte membrane transport functions and oxidative stress during aging in rats

Erythrocyte membrane is a suitable model to study various metabolic and physiological functions as it undergoes variety of biochemical changes during aging. An age-dependent modulatory effect of rapamycin on erythrocyte membrane functions is completely unknown. Therefore, the present study was undertaken to investigate the effect of rapamycin on age-dependent impaired activities of transporters/exchangers, altered levels of redox biomarkers, viz. protein carbonyl (PC), lipid hydroperoxides (LHs), total thiol (–SH), sialic acid (SA) and intracellular calcium ion [Ca2+]i, and osmotic fragility of erythrocyte membrane. A significant reduction in membrane-bound activities of Na+/K+-ATPase (NKA) and Ca2+-ATPase (PMCA), and levels of –SH and SA was observed along with a simultaneous induction in Na+/H+ exchanger (NHE) activity and levels of [Ca2+]i, PC, LH and osmotic fragility in old-aged rats. Rapamycin was found to be a promising age-delaying drug that significantly reversed the aging-induced impaired activities of membrane-bound ATPases and altered levels of redox biomarkers.

Effect of Gestational Intake of Fisetin (3,3',4',7-Tetrahydroxyflavone) on Developmental Methyl Mercury Neurotoxicity in F1 Generation Rats.

Methyl mercury (MeHg) is a developmental neurotoxin that causes irreversible cognitive damage in offspring of gestationally exposed mothers. Currently, no preventive drugs are established against MeHg developmental neurotoxicity. The neuroprotective effect of gestational administration of a flavanoid against in utero toxicity of MeHg is not explored much. Hence, the present study validated the effect of a bioactive flavanoid, fisetin, on MeHg developmental neurotoxicity outcomes in rat offspring at postnatal weaning age. Pregnant Wistar rats were simultaneously given MeHg (1.5mg/kg b.w.) and two doses of fisetin (10 and 50mg/kg b.w. in two separate groups) orally from gestational day (GD) 5 till parturition. Accordingly, after parturition, on postnatal day (PND) 24, weaning F1 generation rats were studied for motor and cognitive behavioural changes. Biochemical and histopathological changes were also studied in the cerebral cortex, cerebellum and hippocampus on PND 25. Administration of fisetin during pregnancy prevented behavioural impairment due to transplacental MeHg exposure in weaning rats. Fisetin decreased the levels of oxidative stress markers, increased enzymatic and non-enzymatic antioxidant levels and increased the activity of membrane-bound ATPases and cholinergic function in F1 generation rats. In light microscopic studies, fisetin treatment protected the specific offspring brain regions from significant morphological aberrations. Between the two doses of fisetin studied, 10mg/kg b.w. was found to be more satisfactory and effective than 50mg/kg b.w. The present study shows that intake of fisetin during pregnancy in rats ameliorated in utero MeHg exposure-induced neurotoxicity outcomes in postnatal weaning F1 generation rats.

Hepatoprotective efficacy of gallic acid during Nitrosodiethylamine-induced liver inflammation in Wistar rats

Gallic acid (GA), a popular phenolic acid is found in gallnuts, grapes, pomegranates, tea and oak bark. It possesses anti-cancer, anti-bacterial, anti-depressant, anti-asthmatic and anti-obesity effects. N′-Nitrosodiethylamine (NDEA) is a well-known hepatotoxin, carcinogen and mutagen. In this study, we have examined the hepatoprotective effect of gallic acid against liver inflammation induced by NDEA in Wistar rats. Hepatic damage in the animals was induced by 10mlkg−1b.wt of 1% NDEA (i.p.) solution in normal saline once in a week. Another group received GA supplement (i.p.) in 100mgkg−1b.wtwk−1. Animals belonging to control group were administered equal amounts of saline or GA. LPO, SOD and membrane-bound ATPase (Ca2+- and Mg2+-ATPase) activities were determined in liver homogenate of control and treated rats. Alterations in liver architecture were assessed by H&E and Masson’s trichrome stainings of 5μm thick liver sections. Immunohistochemistry (IHC) was performed to localize the inflammatory marker, Cyclooxygenase-2 (COX-2). Our results demonstrate a significant increase in malondialdehyde, and decrease in SOD and ATPases (Ca2+/Mg2+) in NDEA-treated rats. Histopathology data showed inflammation, activated HSCs, deposition of collagen, periportal as well as bridging fibrosis in NDEA-treated liver specimens. Immunohistochemistry of NDEA-treated liver sections exhibited COX-2 positive cells. Gallic acid supplement revert the hepatic functioning in rats injured with NDEA probably by inducing Nrf2-mediated antioxidant enzymes and attenuating the inflammatory mediators COX-2 through NF-κB inhibition pathway. Therefore, gallic acid supplement may be a useful promising bioagent in combating liver injury.

Modulatory effect of Tinospora cordifolia extract on Cd-induced oxidative stress in Wistar rats

BackgroundCadmium (Cd), a nonessential heavy metal, is a major environmental and public health concern. Oxidative stress plays an important role in Cd-induced kidney dysfunction. Tinospora cordifolia, a medicinal plant rich in phytochemicals, possesses antioxidant activity. The objective of the present study was to assess the protective effect of Tinospora cordifolia-stem methanolic extract (TCE) on Cd-induced nephrotoxicity in Wistar rats. MethodsMale Wistar rats were administered ∼5mg/kg body weight Cd orally and 100mg/kg body weight TCE for 28 days. At the end of Cd and TCE treatment, biochemical assays were performed in serum and tissue homogenate. ResultsCd-induced oxidative stress in the kidney resulted in increased levels of lipid peroxidation and protein carbonyl content with a significant decrease in cellular antioxidants, such as reduced GSH, SOD, CAT, GPX, and GST. Cd-induced nephrotoxicity was further confirmed by marked changes in the histology of the kidney and increased levels of kidney markers. Additionally, Cd-treated rats showed alterations in membrane-bound ATPase activity and decreased levels of tissue glycoproteins. Cotreatment with TCE considerably reduced the biochemical alterations in serum and renal tissue induced by Cd, and also restored ATPase activity and glycoproteins to near normal levels. ConclusionOur results suggested that TCE with its antioxidant effect offered cytoprotection against Cd-induced toxicity in kidneys by restoring the altered cellular antioxidants and renal markers. TCE treatment for 28 days reversed ATPase activity and tissue glycoprotein levels. These results revealed the protective effect of TCE on Cd-induced toxicity in kidneys and oxidative stress.

Pterostilbene prevents intestinal ischemia reperfusion injury in wistar rats via modulation of antioxidant defense and inflammation

Purpose: To evaluate the protective mechanisms afforded by pterostilbene against intestinal ischemia/reperfusion ( II/R ) injury in Wistar rats.Methods: Male Wistar rats were divided into 4 groups as follows: Control group; intestinal ischemia/reperfusion (II/R) group; pterostilbene only group (20 mg/kg) of body weight and pterostilbene followed by intestinal ischemia/reperfusion (II/R) treated group. The study evaluated oxidative stress markers, including reactive oxygen species (ROS) and lipid peroxide levels, protein carbonyl content, antioxidant status (superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glutathione content) and membrane-bound ATPase activity. The levels of pro-inflammatory mediators, including nuclear factor- kappa B (NF-κB), cyclooxygenase-2 (COX-2) and inflammatory cytokines (TNF-α and IL-1β), were also evaluated.Results: The results showed that pterostilbene (20 mg/kg) followed by intestinal ischemia/reperfusion (II/R) significantly lowered the level of lipid peroxidation (41.33 %), protein carbonyl content (PCC, 44.18 %) and ROS (29.14 %) (p < 0.001) but significantly restored membrane-bound ATPase activities (Ca2+ATPase, 30.76 %; Na+/K+ATPase, 21.42 %; Mg2+ATPase, 30.06 %) (p < 0.003), compared with rats induced with II/R. Furthermore, pterostilbene significantly down-regulated NF-κB and COX-2 expressions (30 %, p < 0.05) compared to rats with II/R injury.Conclusion: The study reveals that pterostilbene offers significant protective activity in rats owing to its antioxidant and anti-inflammatory properties.

Oxidative stress induced by cadmium in the plasma, erythrocytes and lymphocytes of rats: Attenuation by grape seed proanthocyanidins.

The present study has been designed to investigate the ameliorative effect of grape seed proanthocyanidins (GSP) on cadmium (Cd)-induced oxidative damage in rat erythrocytes. Twenty four male Wistar rats were divided into four groups: control, GSP-treated group (100 mg kg(-1) body weight (BW)), Cd-treated group (cadmium chloride, 5 mg kg(-1) BW), and GSP + Cd-treated group in which GSP was orally pre-administered 90 min before Cd intoxication for 4 weeks. At the end of the experimental period, blood samples were collected by cardiac puncture and were processed for various biochemical estimations. The extent of oxidative damage in isolated rat erythrocyte membrane was assessed by measuring lipid peroxidation, enzymatic and non-enzymatic content, calcium ion (Ca(2+))/magnesium ion (Mg(2+))-ATPase and sodium ion (Na(+))/potassium ion (K(+))-ATPase activities, free iron, calcium, hydrogen peroxide (H2O2) concentration, and osmotic fragility. Our results unveiled that Cd intoxication significantly increased the erythrocyte lipid peroxidation markers and decreased the activity of enzymatic and non-enzymatic markers in erythrocytes. Conversely, GSP pretreatment significantly prevented the decrease in the activities of antioxidant enzymes and membrane-bound ATPases. GSP also restored the levels of iron, calcium, and H2O2 in Cd-treated rats. Conformational changes in erythrocytes of various groups were also determined using morphological and ultrastructural electron microscopic analysis. The findings of our study clearly revealed that GSP affords superior protection against Cd-induced reactive oxygen species generation, lipid peroxidation, and free radical generation in Cd-treated rats, which presumably reflects the ability of this flavonoid to protect erythrocytes and lymphocytes of rats from the toxic effects of Cd.

Attenuation of erythrocyte membrane oxidative stress by Sesbania grandiflora in streptozotocin-induced diabetic rats.

The aim of the present study was to investigate the protective effects of Sesbania grandiflora flower (SGF) extract on erythrocyte membrane in Streptozotocin (STZ)-induced diabetic rats. Adult male albino rats of Wistar strain, weighing 190-220 g, were made diabetic by an intraperitonial administration of STZ (45 mg/kg). Normal and diabetic rats were treated with SGF, and diabetic rats were also treated with glibenclamide as drug control, for 45 days. In this study plasma insulin and haemoglobin levels were decreased and blood glucose, glycosylated haemoglobin, protein oxidation, lipid peroxidation markers, and osmotic fragility levels were increased in diabetic rats. Moreover, erythrocytes antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxide, glutathione reductase, glutathione-S-transferase, and glucose-6-phosphate dehydrogenase activities and non-enzymatic antioxidants such as vitamin C, vitamin E, reduced glutathione (GSH), and oxidized glutathione (GSSG) levels were altered. Similarly, the activities of total ATPases, Na(+)/K(+)-ATPase, Ca(2+)-ATPase, and Mg(2+)-ATPase were also decreased in the erythrocytes of diabetic rats. Administration of SGF to STZ-induced diabetic rats reduced blood glucose and glycosylated haemoglobin levels with increased levels of insulin and haemoglobin. Moreover, SGF reversed the protein and lipid peroxidation markers, osmotic fragility, membrane-bound ATPases activities, and antioxidant status in STZ-induced diabetic rats. These results suggest that SGF could provide a protective effect on diabetes by decreasing oxidative stress-associated diabetic complications.

Influence of kaempferol, a flavonoid compound, on membrane-bound ATPases in streptozotocin-induced diabetic rats

Context: Kaempferol is a flavonoid found in many edible plants (e.g. tea, cabbage, beans, tomato, strawberries, and grapes) and in plants or botanical products commonly used in traditional medicine. Numerous preclinical studies have shown that kaempferol have a wide range of pharmacological activities, including antioxidant, anti-inflammatory, anticancer, cardioprotective, neuroprotective, and antidiabetic activities.Objective: The present study investigates the effect of kaempferol on membrane-bound ATPases in erythrocytes and in liver, kidney, and heart of streptozotocin (STZ)-induced diabetic rats.Materials and methods: Diabetes was induced into adult male albino rats of the Wistar strain, by intraperitoneal administration of STZ (40 mg/kg body weight (BW)). Kaempferol (100 mg/kg BW) or glibenclamide (600 µg/kg BW) was administered orally once daily for 45 d to normal and STZ-induced diabetic rats. The effects of kaempferol on membrane-bound ATPases (total ATPase, Na+/K+-ATPase, Ca2+-ATPase, and Mg2+-ATPase) activity in erythrocytes and in liver, kidney, and heart were determined.Results: In our study, diabetic rats had significantly (p < 0.05) decreased activities of total ATPases, Na+/K+-ATPase, Ca2+-ATPase, and Mg2+-ATPase in erythrocytes and tissues. Oral administration of kaempferol (100 mg/kg BW) or glibenclamide (600 µg/kg BW) for a period of 45 d resulted in significant (p < 0.05) reversal of these enzymes' activities to near normal in erythrocytes and tissues when compared with diabetic control rats.Discussion and conclusion: Thus, obtained results indicate that administration of kaempferol has the potential to restore deranged activity of membrane-bound ATPases in STZ-induced diabetic rats. Further detailed investigation is necessary to discover kaempferol’s action mechanism.

Therapeutic efficacy of chlorogenic acid on cadmium-induced oxidative neuropathy in a murine model.

The aim of the present study was to determine whether chlorogenic acid (CA) is able to modulate cadmium (Cd)-induced oxidative brain damage. Cd-treated rats displayed numerous pathological effects, including the inhibition of acetylcholinesterase, elevated lipid peroxidation, the depletion of enzymatic and non-enzymatic antioxidants, the reduction of membrane-bound ATPase activity, mitochondrial dysfunction and DNA fragmentation. Pretreatment of the rats with CA significantly attenuated these effects. These results lead to the hypothesis that the mechanisms by which CA attenuates the effects of Cd-induced oxidative brain damage include the maintenance of antioxidant homeostasis, inhibition of the membrane effects and the perpetuation of mitochondrial dysfunction. These data support the potential of CA as a beneficial intervention in the prevention of heavy metal poisoning due to Cd exposure.

Dietary Chitosan Supplementation Ameliorates Isoproterenol-Induced Aberrations in Membrane-Bound ATPases and Mineral Status of Rat Myocardium.

Myocardial infarction is one of the major public concerns in both developed and developing countries. Recently, there is growing interest in potential healthcare applications of marine natural products in the field of cardiovascular research. In the present study, we have examined the membrane-stabilizing potential of marine mucopolysaccharide-chitosan in modulating the aberrations of thiol-dependent membrane-bound ATPases activities, mineral status, and cardiac diagnostic markers in isoproterenol-induced myocardial infarction condition in rats. Dietary intake of chitosan significantly (p < 0.05) counteracted the isoproterenol-induced lipid peroxidation and maintained the levels of thiol contents and cardiac biomarkers at concentrations analogous to that of normal controls in the rat myocardium. Chitosan administration also significantly mitigated isoproterenol-induced aberrations in the membrane-bound ATPase activities in the heart tissue and preserved the myocardial mineral status in serum and heart tissue of experimental rats at near normal value. The results of the present study haveindicated that the salubrious effect of dietary chitosan supplementation in attenuating the experimentally induced myocardial infarction condition is probably ascribable to its antioxidant defense and membrane-stabilizing properties.

Free radical quenching effect of Shemamruthaa—a Siddha drug in 7,12-dimethylbenz(a)anthracene-induced experimental breast cancer rats

This study aims to evaluate the modulatory effect of Shemamruthaa (SM), a modified indigenous Siddha formulation, on the hematological indices, membrane-bound enzymes, enzymatic antioxidants free radical levels in cancer rats and also on the histologicl alterations in the mammary tissue. Mammary cancer was induced by intragastric administration of a single dose of 25 mg/kg body weight of 7,12-dimethylbenz(a)anthracene (DMBA), and cancer-induced rats were treated with oral administration of SM at a dosage of 400 mg/kg body weight dissolved in water for 14 days. Hematological indices such as hemoglobin (HB), red blood cells (RBC), white blood cells (WBC), platelets counts and packed cell volume (PCV) were decreased, whereas erythrocyte sedimentation rate (ESR) was increased. Moreover, lipid peroxidation and free radicals were found to be increased, whereas activities of antioxidant enzymes and membrane-bound ATPases were decreased in cancer-bearing animals when compared with control rats. The drug SM also effectively restored morphological alterations in the mammary tissue of cancer-bearing rats. From the results of the present study, the beneficial effect of SM on DMBA-induced mammary carcinoma is evident.

Aspartame induces alteration in electrolytes homeostasis of immune organs in wistar albino rats

Aspartame is rapidly and completely metabolized in humans and experimental animals to aspartic acid (40%), phenylalanine (50%) and methanol (10%). Methanol, a toxic metabolite is primarily metabolized by oxidation to formaldehyde and then to formate. These processes are accompanied by the formation of superoxide anion and hydrogen peroxide. This study is focused to understand whether the oral administration of Aspartame (40mg/kg bw) for 15 days, 30 days, and 90 days have any effect on immune organs. Damage to plasma membrane was assessed by levels of membrane-bound ATPases. Oxidative stress status was assessed by alterations in level of lipid peroxides, protein carbonyls, protein thiol and lipid-soluble antioxidant vitamin E. To mimic human methanol metabolism, folate-deficient animals were used. There was decrease in all membrane-bound ATPases activities in immune organs. Aspartame administration to rats inducing excess free radical generation is confirmed by increase in lipid peroxidation, obvious which is also again substantiated by the elevated protein carbonyl and decrease in protein thiol in this study. These excess free radical generations also decrease the cellularity (reduction in organ weight and cell count) of immune organs.

Inhibition of nitrate reductase and ATPase activities in Zea mays roots by tungsten and N, N'-dicyclohexylcarbodiimide

The activity of soluble and membrane-bound ATPase obtained from corn roots was in vivo markedly inhibited by N,N' -dicyclohexylcanbodiimide (DCCD) and W0&lt;sub&gt;4&lt;/sub&gt;&lt;sup&gt;2-&lt;/sup&gt; ions. DCCD (2.5 X 10&lt;sup&gt;-5&lt;/sup&gt; M) added to the nutrient solution strongly decreased in vivo nitrate reductase (NR) activity after 12-h growth of plants while it had no effect in experiments &lt;em&gt;in vitro&lt;/em&gt; on NR activity. Tungsten in a concentration of 10&lt;sup&gt;-4&lt;/sup&gt; M completely blocked NR activity after 24 h. In the above used concentrations neither DCCD nor W0&lt;sub&gt;4&lt;/sub&gt;&lt;sup&gt;2-&lt;/sup&gt; inhibited completely N0&lt;sub&gt;3&lt;/sub&gt;&lt;sup&gt;-&lt;/sup&gt; absorption by corn roots. The results suggest that there must exist in corn roots another or an additional mechanism of N0&lt;sub&gt;3&lt;/sub&gt;&lt;sup&gt;-&lt;/sup&gt; assimilation apart from of that proposed by Butz and Jackson (1977).

Effect of aspartame on lipid peroxidation and membrane bound enzymes in immune organs of rats

Objective: The artificial dipeptide sweetener aspartame (L-aspartyl-L-phenylalanine methyl ester) is present in many products especially unsweetened and sugar products. These products are frequently utilized by people trying to lose weight or patients with diabetes. Concern relating to the possible adverse effect has been raised due to aspartame’s metabolic components. Aspartame is rapidly and completely metabolized in humans and experimental animals to aspartic acid (40%), phenylalanine (50%) and methanol (10%). Methanol, a toxic metabolite, is primarily, metabolized by oxidation to formaldehyde and then to formate: these processes are accompanied by the formation of superoxide anion and hydrogen peroxide. Methods: This study focus is to understand whether the oral administration of aspartame (40 mg/kg body weight) for 90 days has any effect on lipid peroxidation, nitric oxide level, membrane bound ATPases of immune organs and differential leucocyte count of rats. Results: After 90 days of aspartame administration, there was a neutrophil and lymphocyte imbalance in normal white blood cell homeostasis, a significant increase in lipid peroxidation with nitric oxide level, and an alteration of membrane bound ATPase activities, which finally decreased the cellularity (reduction in organ weight and cell count) of immune organs. Conclusion: Aspartame metabolite methanol or formaldehyde may be the causative factors behind the changes observed. This study concludes that oral administration of aspartame for longer duration may cause oxidative stress on immune organs.

Ameliorative effect of diallyl trisulphide on arsenic-induced oxidative stress in rat erythrocytes and DNA damage in lymphocytes

Arsenic (As) is a naturally occurring semimetallic element that is classified as a toxicant and a human carcinogen. Diallyl trisulphide (DATS), an organosulphur compound, is an antioxidative substance that is extracted from garlic (Allium sativum). Erythrocytes are very expedient models to understand the susceptibility of membrane to oxidative damage induced by different xenobiotic compounds. Arsenic has been reported to induce oxidative stress to erythrocytes due to lipid peroxidation and alteration in defence mechanism as erythrocytes are the first target that arsenic compounds attack in the body after systemic absorption. In the light of this fact, the purpose of this study is to characterise the ameliorative effect of DATS on arsenic-induced oxidative stress in rat erythrocytes. Experimental rats were randomly divided into four groups and treated orally for 28 days: control, As [5 mg/kg body weight (BW)] treated, As+DATS (80 mg/kg BW) treated, DATS (80 mg/kg BW) treated and As+vitamin C (100 mg/kg BW) treated. Oxidative stress in erythrocytes was recorded by estimating plasma marker enzymes, plasma and erythrocyte membrane oxidative stress markers, erythrocyte membrane antioxidant enzymes and non-antioxidant enzymes, etc. Oral administration of arsenic at 5 mg/kg BW per day elevated the levels of plasma marker enzymes, namely, aspartate transaminase (AST), alanine transaminase (ALT), acid phosphatase (ACP), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), and γ-glutamyl transferase (γGT) (U/L) with significantly increased lipid peroxidation markers such as thiobarbituric acid reactive substances (TBARS), malondialdehyde (MDA), lipid hydroperoxides (LH), conjugated dienes (CD), and protein carbonyl (PC) contents were also elevated in As-treated rat plasma and erythrocytes. The levels of non-enzymatic antioxidants (reduced glutathione, vitamins C and E) and enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G6PD) were also decreased in As-treated rats. The toxic effect of As significantly decreased the activities of membrane-bound ATPases (Na+/K+-ATPase, Mg2+-ATPase, and Ca2+-ATPase), with a significant increase in% tail DNA of rat lymphocytes measured by means of a single-cell gel electrophoresis assay. Administration of DATS for 28 days significantly reduced the levels of plasma markers. The levels of TBARS, MDA, LH, CD, and PC were significantly decreased and there was a significant increase in ATPase activities and non-enzymatic and enzymatic antioxidants on treatment with DATS in a dose-related manner. All these changes were supported by reduction of DNA damage in lymphocytes with DATS treatment. DATS at a dose of 80 mg/kg BW was found to be most effective and the results revealed the same. The results of the study showed that DATS shows a protective effect against As-induced oxidative stress in rat erythrocytes and lymphocytes.

Oral treatment with gallic acid and quercetin alleviates lindane-induced cardiotoxicity in rats

Lindane is a man-made organochlorine pesticide used for agricultural purposes. Since lindane-induced toxicity is mediated by free radical generation, this investigation was carried out to study the protective effects of gallic acid and quercetin against lindane-induced cardiotoxicity. Lindane (100 mg·(kg body mass)(-1)) was administered orally to rats for 30 days. Histological analysis revealed pathological changes in the heart of lindane-treated rats. Biochemical analysis of the lindane-treated animals showed elevated activity for serum marker enzymes, lipid peroxidation (LPO), and membrane-bound Ca(2+) ATPase, with a concomitant decrease in the level of non-enzymic antioxidant (GSH), enzymic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase (GPx), and glutathione-S-transferase (GST), and membrane-bound ATPases like Na(+)/K(+) ATPase and Mg(2+) ATPase in heart tissue. The results suggest that gallic acid and quercetin offer protection against lindane-induced myocardial damage, possibly through maintaining levels of endogenous antioxidant enzymes and membrane bound ATPase activity, as well as inhibiting lipid peroxidation.