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  • Some alterations in the integrity of cell membranes caused b

    2022-11-05

    Some alterations in the integrity of cell membranes caused by toxic agents can be determined by measuring certain enzymes released by damaged cells [8]. The cholinesterases, for example, catalyze the hydrolysis of Dacarbazine (ACh) in choline and acetic acid. Theses enzymes are divided into two types: the acetylcholinesterase (AChE; EC 3.1.1.7) and butyrylcholinesterase (BChE; EC 3.1.1.8). These enzymes play important roles during the immune and inflammatory responses, due to ACh anti-inflammatory effect [9]. Recently, some studies have reported that BChE is a novel marker of tissue inflammation and acute inflammatory response [10]. The adenosine deaminase (ADA) is another important enzyme used as marker of tissue damage, being considered a key enzyme in the purine metabolism, catalyzing the deamination of adenosine and deoxyadenosine to inosine and deoxyinosine, respectively, by regulating the concentration of extracellular adenosine [11]. ADA activity plays an important role on immune and inflammatory response by regulating adenosine levels, a molecule of the anti-inflammatory process, and thus, protecting the host tissue from damage [12]. Considering tissue damage caused by aflatoxins in intoxicated animals and taking into account that their mechanisms of action are not yet fully understood, the aim of this study was to assess whether aflatoxins in the diets used to feed quails (Coturnix coturnix) could influence cholinesterases and ADA activities.
    Materials and methods
    Results
    Discussion In this study, alterations in the activities of enzymes involved in the regulation of acetylcholine, butyrylcholine and adenosine levels were found in quails intoxicated by aflatoxins. Probably, these changes occur due to the inflammatory process as proved by the presence of gross lesions and microscopical hepatic alterations such as mentioned in the literature [22]. The histopathological alterations in the liver of quails fed with aflatoxins have been reported in the literature by many authors [23], [24], as well as recently reported in chickens [25], [26]. The cytoplasmic vacuolization might be a result of the inhibition of protein synthesis in the hepatic tissue [22]. We observed that AChE and BChE activities increased in the groups fed with aflatoxins, in disagreement with other studies, where the cholinesterases were inhibited [27], [28], [29]. According to Hasmann et al. [29], the reduction on cholinesterases occurs because of the effect of aflatoxin on peripheral sites of AChE and BChE. However, the increase of AChE and BChE activities might be explained by the toxic effect of aflatoxins in the liver tissue, where they are biotransformed by the hepatic microsomal system in very toxic metabolites, such as aflatoxin B2 and 2,3-epoxide AFL. Also, with increased AChE activity, more ACh is hydrolyzed, which contributes to the inflammatory process since it decreases ACh levels, an important anti-inflammatory molecule [9]. According to Sakata et al. [30], these reactive metabolites bind covalently to DNA and RNA molecules, altering the protein synthesis in the hepatic tissue, leading to an exacerbated expression and, consequently, increased production of AChE and BChE. The histopathological analyses demonstrated severe microvacuolar degeneration in the hepatic tissue of animals fed with aflatoxins, which may explain the reduction in the levels of plasmatic proteins, and consequently, increased cholinesterases activities [31]. Recently, a study demonstrated a reduction in ADA activity in chickens intoxicated by other mycotoxins, such as ochratoxin, zearalenone, and deoxynivalenol [32], differently from what was observed in this study. ADA enzyme is responsible for regulating the adenosine levels, an anti-inflammatory molecule, that acts as a sensor to immune system during tissue damage and acute inflammation [26]. The increase in ADA activity in serum, liver and brain observed in this study could contribute to cell damage and to the inflammatory process because it would decrease adenosine levels, an anti-inflammatory molecule [33].