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Cyanide, in the environment, has been associated with many intoxication episodes in humans and animals resulting from the ingestion of foods, environmental pollution, chemical war, suicide, homicide, occupational factors and use in some drugs such as nitroprusside and laetrile (Tulswani et al. , 2005). Cyanide concentrates in erythrocytes through binding to methemoglobin (Tulswani et al. , 2005). Subacute oral administration of cyanide in rats produced changes in several biochemical indices and pathology in various organs (Tylleskar et al. , 1991). The purpose of this study was to determine the antioxidant property of aqueous extract A. sceptrum in some oxidative stress markers and antioxidants biochemical parameters in rats exposed to cyanide. The results in the study from fig. 1 aboverevealed that the PCV and Hb level weresignificantly (p < 0. 05) decreased in cyanide control rats as compared to normal controlandall other groups. The decreased in haematocrit value, in cyanide exposed animals indicate destruction of erythrocytes (Dede et al. , 2002). Fariss (1991) had earlier reported that antioxidants are useful in protecting against chemical toxicity.
The supplementation of the food with A. sceptrum extracts decrease the toxic effect of cyanide on the haematological values and has a protective role in anaemia and illness. This is because administration of the A. sceptrum extract tends to restore haematological parameters (PCV and Hb) near control values. The protective role was more effective with 20mg/kg body weight of A. sceptrum extract as simultaneously compare to 10mg/kg body weight of A. sceptrum. The decreased serum levels of albumin and total protein in the present study (Table 2) would indicate possible hepato-toxic effects of cyanide exposure in rats that is reminiscent of previously reported pathological and biochemical findings in several animal species exposed to cyanide (Okolie andIroanya, 2003; Tulsawani et al. , 2005). As shown in the results, the observed changes were mitigated in the rats treated with the aqueous extract of A. sceptrum in comparison to the group not treated (cyanide control), which indicates that the A. sceptrum extract has capability of providing some protection against cyanide induced tissue damage. In this study, alkaline phosphatase (ALP), aspartate aminotransferase (AST), and alanine amino transferase (ALT) activities were found to be increased following cyanide exposure (Tables 2 & 3). This is in line with Okolie and Osagie (1999) who stated that sublethal cyanide poisoning increases serum AST activity in rats. Similar results were found in study conducted by Elsaid and Elkomy (2006) which showed significant increases of ALP, AST and ALT enzyme activities in rats drinking water contaminated with cyanide. It is well known that the ALP, AST and ALT are very active in the liver, hence they are marker enzyme and damage to the liver may lead to its increase in the serum.
From the results it may suggest that A. sceptrum is an effective antidote for cyanide toxicity because it decreases the level of serum and liver ALP, AST and ALT activities after administration to cyanide poisoned rats in comparison to rats poisoned with only cyanide. However, oral administration ofA. sceptrum to the rats not exposed to cyanide, the ALP, AST and ALTactivitiesin the serum and the liverwas also enhanced but this were notsignificant when compared to the normal control. There are many documents in the literature on the effect of cyanide on the antioxidant enzymes systems in different cells and tissues of animals. SOD catalyses the dismutation of superoxide radical to hydrogen peroxide, which is then converted to water by GPx or by catalase (Nikoli-Kokic et al. , 2010). Based on the present study results, prolonged sublethal cyanide administration caused significant decrease in the mean value of serumand liver SOD, CATand liver GPx,activities as compared to control group. The reduction of SOD and CAT in the serum and liver of the cyanide treated rats (Tables 3 & 4)is somewhat similar with the previous reports indicating the reduction of SOD and catalase activities in some tissues of cyanide toxified rats and rabbits (Okolie and Osobase, 2005). The decreased SOD activity may be attributed to irreversible inactivation of this enzyme by its product, H2O2, due to cyanide-induced increase in superoxide anion generation ((Nikoli-Kokic et al. , 2010) or directly to its irreversible inhibition by cyanide (Okolie and Osobase, 2005). On the other hand, the higher activity of serum and liver SOD, CAT and liver GPx in cyanide exposed rats treated with the aqueous extract of A. sceptrum might be as a compensatory response to enhanced ROS formation and may supply more protection against free radical-mediated oxidative damages. GSH help in the removal of hydrogen peroxide by the GPx-catalysed reaction (Konukoglu et al. , 1998). It has been reported that cyanide poisoning in rats significantly decreased reduced glutathione in the blood, liver and brain (Mathangi et al. , 2011). Also, acute exposure of lethal dose of cyanide was found to decline GSH levels in the liver of rats (Mathangi et al. , 2011). However, the lower blood reduced GSH in the cyanide toxified rats in comparison with the normal controls (Table 3) is in line with the work of Mathangi et al. , 2011 who indicated significant reduction in erythrocytic GSH concentration in cyanide toxified rats. Based on the present results, significant enhancement of MDA values were observed in the serum and liver of cyanide-intoxicated rats. In line with the findings, the results of Mathangi et al. (2011) showed that oral administration of cyanide to rats for 90 days caused increased lipid peroxidation in the brain and liver.
The administration of A. sceptrum aqueous extract contributed to lowering serum and liver MDA levels when compared with normal control group. No significant difference was observed in the liver MDA level in 10mg/kg body weight of A. sceptrum aqueous extractand 20mg/kg body weight of A. sceptrum aqueous extract in comparison with the normal control. This is in agreement with previous investigation conducted by George et al. (2012). The administration of A sceptrum tend to normalized liver MDA level (George et al. , 2013; George et al. , 2012). In figure 2, the normal control showed normal hepatic cells and broad central vein, the cyanide control showed ballooning degradation and severe hepatic necrosis. Treatment of the Cyanide exposed rats with 10mg/kg body weight and 20mg/kg body weight aqueous extract of A. sceptrum, showed a reduction in hepatic necrosis and ballooning degradation. Treatment of the Normal rats with 10 and 20 mg/kg body weight of aqueous extractofA. sceptrum, showing hepatic cells prominent nucleus, no hepatic necrosisThebasis of the results of this study,may be due to the possible mechanism of hepatoprotective effect through antioxidant activity of A. sceptrum (George et al. , 2012). Erukainure et al. , 2011 stated that the antioxidant activity of A. sceptrum might be due to the presence of active constituents such as flavonoids, and quinones. ConclusionAqueous extract of A. sceptrumexerts effects not only by modulating lipid peroxidation but it also acts as enhancing the antioxidant and detoxifying enzyme systems. Oral administration ofaqueous extract of A. sceptrum10mg/kg bwtand 20mg/kg bwtthree times per weekfor 28 days havea promising role and it worth to be considered as an antidote for cyanide toxicity.
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