Individual in vitro effects of ochratoxin A, deoxynivalenol and zearalenone on oxidative stress and acetylcholinesterase in lymphocytes of broiler chickens

Abstract

The contamination of consumer food and animal feed with toxigenic fungi has resulted in economic losses worldwide in animal industries. Mycotoxins are highly biologically reactive secondary metabolites and can inhibit protein synthesis and cell multiplication. Considering the cytotoxicity of mycotoxins, this experiment was performed to determine the in vitro influence of ochratoxin A, deoxynivalenol and zearalenone on lipid peroxidation in lymphocytes of broiler chickens at different concentrations. This study has also evaluated whether the presence of these mycotoxins changes the acetylcholinesterase activity in lymphocytes, which is involved in the regulation of immune and inflammatory responses. Blood lymphocytes of broiler chickens were isolated through density gradient centrifugation and incubated with the respective mycotoxins at concentrations of 0.001, 0.01, 0.1 and 1 μg/mL. Lipid peroxidation, which was evaluated through the amount of malondialdehyde measured in a thiobarbituric acid-reactive species test, and the enzymatic activity were analyzed at 24, 48 and 72 h. Results of the lipid peroxidation evaluation showed an increasing cytotoxicity relation: ochratoxin A > deoxynivalenol > zearalenone. Conversely, cytotoxicity was valued as zearalenone > deoxynivalenol > ochratoxin A in relation to the acetylcholinesterase enzymatic activity. At a concentration of 1 μg/mL, ochratoxin A and deoxynivalenol induced the highest cellular oxidative stress levels and the highest enzymatic activity at the majority of time points. However, the same mycotoxins, except at 1 μg/mL concentration, induced a reduction of lymphocytic lipid peroxidation 72 h after incubation, suggesting the action of a compensatory mechanism in these cells.

Effectiveness of activated carbon and Egyptian montmorillonite in the protection against deoxynivalenol-induced cytotoxicity and genotoxicity in rats

“…Moreover, a previous report indicated that DON and other mycotoxins are activated by the hepatic cytochrome P 450 enzyme system to produce a highly reactive intermediates which subsequently binds to nucleophilic sites in DNA forming an adduct (Awad et al, 2012). Consequently, the formation of DON-DNA adducts is regarded as a critical step in the initiation of DON-induced hepatocarcinogenesis (Lautert et al, 2014). The results reported herein also revealed that treatment with DON induced DNA fragmentation in liver.…”

Limited Link between Oxidative Stress and Ochratoxin A—Induced Renal Injury in an Acute Toxicity Rat Model

“…Based on the previous studies, the mechanisms of OTA were explored [7,8,9,35,36,37]. Oxidative stress has an important role in vitro.…”

“…OTA displays nephrotoxicity [4], hepatotoxicity [1], carcinogenicity [5], and neurotoxicity [6] in mammals. There are some studies that have revealed the mechanisms of OTA, such as, protein synthesis inhibition [7], lipid peroxidation [8], mitochondrial function inhibition [9], DNA methylation [10], miRNA regulation [11], the changes of enteric microorganism [12], renal cortex fibrosis, and epithelial-to-mesenchymal transition [13,14] etc. Some researchers also suggested that the toxicity is related to oxidative stress, and other researchers insist that DNA damage, including DNA adduct formation and DNA strand breaks, are responsible [15,16,17].…”

Cytotoxic Effects of Ochratoxin A in Neuro-2a Cells: Role of Oxidative Stress Evidenced by N-acetylcysteine

“…Earlier studies have shown that alteration in AChE activity is one of the main causes for AD ( Talesa, 2001 ). Lautert et al (2014) showed that OTA induced acetylcholine esterase (AChE) activity which led to increased cellular oxidative stress levels. A member of the neurotrophin family, brain-derived neurotrophic factor (BDNF) directs neuronal cell survival, promotes growth and differentiation in the developing nervous system.…”