Protective Role of Moringa oleifera (Sajina) Seed on Arsenic-Induced Hepatocellular Degeneration in Female Albino Rats
ABSTRACT In an attempt to develop new herbal therapy, an aqueous extract of the seed of Moringa oleifera was used to screen the effect on arsenic-induced hepatic toxicity in female rat of Wistar strain. Subchronic exposure to sodium arsenite (0.4 ppm/100 g body weight/day via drinking water for a period of 24 days) significantly increased activities of hepatic and lipid function markers such as alanine transaminase, aspartate transaminase, cholesterol, triglycerides, LDL along with a decrease in total protein and HDL. A notable distortion of hepatocellular histoarchitecture was prominent with a concomitant increase in DNA fragmentation following arsenic exposure. A marked elevation of lipid peroxidation in hepatic tissue was also evident from the hepatic accumulation of malondialdehyde and conjugated dienes along with suppressed activities in the antioxidant enzymes such as superoxide dismutase and catalase. However, co-administration of aqueous seed extract of M. oleifera (500 mg/100 g body weight/day for a period of 24 days) was found to significantly prevent the arsenic-induced alteration of hepatic function markers and lipid profile. Moreover, the degeneration of histoarchitecture of liver found in arsenic-treated rats was protected along with partial but definite prevention against DNA fragmentation induction. Similarly, generation of reactive oxygen species and free radicals were found to be significantly less along with restored activities of antioxidant enzymes in M. oleifera co-administered group with comparison to arsenic alone treatment group. The present investigation offers strong evidence for the hepato-protective and antioxidative efficiencies of M. oleifera seed extract against oxidative stress induced by arsenic.
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ABSTRACT: 28 Arsenic (As) is a well-known human carcinogen and a potent hepatotoxin. Environmental exposure to 29 arsenic imposes a serious health hazard to humans and other animals worldwide. Tetrahydrocurcumin 30 (THC), one of the major metabolites of curcumin, exhibits many of the same physiological and pharmaco-31 logical activities as curcumin and in some systems may exert greater antioxidant activity than the cur-32 cumin. It has been reported that THC has antioxidant efficacy attributable to the presence of identical 33 b-diketone of 3rd and 5th substitution in heptane moiety. In the present study, rats were orally treated 34 with arsenic alone (5 mg kg-1 bw/day) with THC (80 mg kg-1 bw/day) for 28 days. Hepatotoxicity was 35 measured by the increased activities of serum hepatospecific enzymes, namely aspartate transaminase, 36 alanine transaminase, alkaline phosphatase and bilirubin along with increased elevation of lipid 37 peroxidative markers, thiobarbituric acid reactive substances. And also elevated levels of serum choles-38 terol, triglycerides, free fatty acids and phospholipids were observed in arsenic intoxicated rats. These 39 effects of arsenic were coupled with enhanced mitochondrial swelling, inhibition of cytochrome c oxi-40 dase, Ca 2+ ATPase and a decrease in mitochondrial calcium content. The toxic effect of arsenic was also 41 indicated by significantly decreased activities of enzymatic antioxidants such as superoxide dismutase, 42 catalase, and glutathione peroxidase along with non-enzymatic antioxidant such as reduced glutathione. 43 Administration of THC exhibited significant reversal of arsenic induced toxicity in hepatic tissue. All these 44 changes were supported by the reduction of arsenic concentration and histopathological observations of 45 the liver. These results suggest that THC has a protective effect over arsenic induced toxicity in rat. 46Chemico-Biological Interactions 04/2015; · 2.98 Impact Factor
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ABSTRACT: Present study demonstrates the therapeutic role of Emblica officinalis (EO) against arsenic-induced DNA and hepatic damage in female rats. Our earlier study on arsenic-exposed human unveils a link between tissue necrosis and carcinogenesis with impaired antioxidant system-associated DNA damage. Here we show ingestion of EO extract (500 mg in 0.1 mL water) in combination with sodium arsenite (0.4 ppm)/100 g b.w. for 24 days to rats offered significant protection against arsenic-induced oxidative damages of DNA and hepatic tissue architecture. Arsenic only exposure decreased hepatic superoxide dismutase, catalase activities and the level of non protein soluble thiol with a concomitant increase in thiobarbituric acid reactive substances and conjugated di-enes which are restrained by EO with a restoration of antioxidant components. In conclusion, restricted generation of free radicals is correlated to DNA protection resulting in prevention of tissue necrosis and possible carcinogenesis.Molecular and Cellular Toxicology 03/2014; 10(1-1):75-82. DOI:10.1007/s13273-014-0009-8 · 0.83 Impact Factor
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ABSTRACT: This study elucidates the protective role of Green tea (Camellia sinensis or CS) against arsenic-induced mutagenic DNA-breakage/intestinal (small) damages in female rats. Intestinal epithelial cells receive ingested arsenic initially. Though, the possibility of damages in this tissue is immense and the therapeutic strategies against this damage are of great concern, reports on either issue are scanty. Our earlier study on arsenic-exposed human unveils a link between carcinogenesis and mutagenic DNA damage. Here, we demonstrate that supplementation of CS-extract (10 mg/mL water) with NaAsO2 (0.6 ppm)/100 g b.w. for 28 days to rats offered a significant protection against arsenic-induced oxidative damages to DNA and intestinal (small) tissues by buttressing antioxidant systems. Necrotic and apoptotic damages and their CS-protection are shown in DNA-fragmentation, comet-assay, and histoarchitecture (hematoxylin and eosin and periodic acid-schiff staining) results. Only arsenic exposure significantly decreased intestinal superoxide dismutase, catalase activities, and level of soluble thiol with a concomitant increase in malondialdehyde/conjugated dienes. Alteration of serum necrotic marker lactate dehydrogenase and the metabolic inflammatory marker c-reactive protein also indicate the impairment may be occurring at transcription and/or cellular signal transduction level. In addition, in situ incubation in rat intestinal loop filled for 24 h with NaAsO2 alone (250 µM) or with aqueous CS-extract (250 mg/mL) suggests that small intestinal epithelial cells are significantly protected by CS against arsenic-associated necrotic/mutagenic damages, which is observed in DNA-breakage studies. In conclusion, besides intensifying endogenous antioxidant system, CS polyphenols also offer a direct role on free radical scavenging activity that is associated to the protection from mutagenic DNA-breakages and prevention of tissue necrosis/carcinogenesis generated by arsenic. © 2014 Wiley Periodicals, Inc. Environ Toxicol, 2014.Environmental Toxicology 03/2014; DOI:10.1002/tox.21977 · 2.56 Impact Factor