Environmental cyanide, has been noted for its’ association with many deadly incidents in living organisms, especially humans via food consumption, drugs and non-conventional means (Tulswaniet al., 2005; Abraham et al., 2016). Cyanide concentrates in erythrocytes through binding tomethemoglobin (Baud et al., 2002). Subacute cyanide exposures in rats have been previously reported to produce changes using several biochemical pathological indices (Tylleskaret al., 1991). This study investigated the potency of ASAE as an antidote for cyanide virulence via utilization of several antioxidant and oxidative metabolic stress indices.
The significant decrease in the PCV and Hb level in cyanide control rats relative to normal control and other groups could be traced to the significant increased destruction of erythrocytes due to cyanide (Dedeet al., 2002).Information in literature indicated the antioxidants protect animals from noxious chemicals (Fariss, 1991). Thus treatment with ASAEwas observed to have reducedthe noxious effects impacted by cyanide on haematological parameters and may be said to possess anti-anaemic potentials. The justification of this claim is that ASAE therapy restored haematological parameters (PCV and Hb) near control values with the 20mg/kg body weight dose being more potent than the 10mg/kg body weight dose. Reduction in the protein levels of serum and liver observed in tables 2 & 3 may be indicative of possible hepato-toxic anomalies of cyanide exposure in rats that is reminiscent of previously reported pathological and biochemical findings in several animal and human models of cyanide insult (Okolie and Iroanya, 2003; Tulsawaniet al., 2005; Dhaset al., 2011). These reductions however were mitigated by ASAEin comparison to the non-treated group (cyanide control).
Also the liver function enzymes activities were found to be increased in the serum and liver following cyanide exposure (Tables 2 & 3). These observations are in consonance with an earlier study by Okolie and Osagie (1999) who stated that sublethal cyanide poisoning has the ability to increase serum AST activity in rats. Similar results were found in the study conducted by Elsaid and Elkomy (2006), Hyl’nezaket al., (1980); Chandra et al., (1980) that also indicated noticeable rise of ALP and the transferases in rats drinking water contaminated with cyanide. It is an established truth that these enzymes have very high liver activities, hence they are often used as significant marker enzymes for status of liver integrity and damage especially in cases where they rise above normal limits in the serum. Based on the reported decline and stability of the levels of liver proteins and enzyme activities after dosing with ASAE, it may be suggested that ASAE is an effective antidote for cyanide noxiousness and has the capability of providing some level of protection against cyanide induced liver damage. A significant observation that was observed is stability in the levels of total protein, albumin and eventual insignificant rise of the liver enzymes in rats treated with only the plant extracts compared to control. This gives credence to an earlier report on the ability of plant materials to confer protection on hepatocellular damage during cyanide intoxication (Kadiri, 2017).
There are many documents in the literature about cyanide and antioxidant enzymes systems in different cells and animal tissues which has established that SOD catalysesdismutation of several superoxide radicals to hydrogen peroxide and eventually converted to water by GPx or by catalase (Nikoli-Kokicet al., 2010; Weydert and Cullen, 2010). Based on this results, prolonged sublethal cyanide administration caused significant depletion in the mean value of serum and liver antioxidant enzyme, activities as compared to control group (Tables 3&4) and is somewhat similar with the previous reports indicating the reduction of SOD and catalase activities in some tissues of cyanide intoxicated 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-Kokicet al., 2010) or directly to its irreversible inhibition by cyanide (Okolie and Osobase, 2005). Conversely, higher activities of serum and liver SOD, CAT and liver GPx in cyanide intoxicated rats which were later treated with ASAEs might be a compensatory response to enhanced ROS formation and may supply more protection against free radical-mediated oxidative damages. GSH help in the removal of peroxides of hydrogen by the GPx-catalysed reaction (Konukogluet al., 1998). Reports indicate cyanide poisoning depreciates GSH in liver, brain and blood of rats (Mathangiet al., 2011). Also, acute insult of lethal dose of cyanide reportedly led to a downturn in liver and serum GSH levels of cyanide intoxicated rats thus in comparison with the normal controls (Table 3) this is in tandem with the works of Okaforet al., (2006); Bhattacharya, et al., (2002) Mathangiet al., 2011 who also observed very significant cutback in erythrocytic GSH assemblage in cyanide treated rats.
As shown by the results, enhancement of MDA values was perceived in cyanide-intoxicated rats. In line with these submissions, Mathangiet al. (2011) showed that 90 days cyanide exposure to rats heightened lipid peroxidation in liver and brain cells. The trend reversibility of heightening MDA levels by A. sceptrumcomparable to control groups 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 and Osioma., 2012). The observed reversal of the altered tissue ultra-structure evidenced by reduced tissue necrosis and ballooning in cyanide exposed rats by 10mgKg-1and 20mgKg-1 of A.sceptrumextracts (fig. 2) may be likened to possible mechanisms of their hepatoprotective efficacy of the rich antioxidants and active constituents such as flavonoids, and quinones. (George et al., 2012; Erukainureet al., 2011).
Themechanistic modulation of the reactive oxygen generating system by ASAE at 10mg/kg and 20mg/kg weight dose and its buffering capacity for the enhancement of the detoxifying and defense enzyme systems makes it a potential standard remedy of cyanide noxiousness.