Oxidative stress mediated the inhibition of cerebral creatine kinase activity in silver catfish fed with aflatoxin B1-contaminated diet

Abstract

Aflatoxin B (AFB) is an environmental toxicant and neurotoxic compound that induces the production of free radicals, causing oxidative stress. Creatine kinase (CK) is a central controller of energy metabolism in tissues with a large and fluctuating energy demand, and it is highly susceptible to inactivation by free radicals and oxidative damage. Thus, the aim of this study was to evaluate whether a diet for freshwater silver catfish (Rhamdia quelen) containing AFB inhibits cerebral CK activity, as well as the involvement of the oxidative stress on this inhibition. Brain CK activity was lower on days 14 and 21 post-feeding in animals that received AFB-contaminated diet compared to the control group (basal diet), similarly to the brain sodium-potassium pump (Na, K-ATPase) activity. On the other hand, lipid peroxidation and protein carbonylation levels were higher on days 14 and 21 post-feeding in animals fed with AFB-contaminated feed compared to the control group, while the antioxidant capacity against peroxyl radicals and thiol content was lower. Based on these evidences, the data demonstrated that diet containing AFB severely affects CK activity, an essential enzyme that plays an important role in brain energy homeostasis. Also, the impairment of energetic homeostasis linked with the use and generation of ATP via inhibition of CK activity elicited an inhibition of enzymes ATP-dependent, such as Na, K-ATPase. Moreover, the inhibition of brain CK activity appears to be mediated by the oxidation of lipids, proteins, and thiol group, as well as by a reduction in the antioxidant capacity.

The Novel Neurotoxic and Neuroimmunotoxic Capabilities of Aflatoxin B1 on the Nervous System: A Review

“…Studies have shown that AFB1 directly binds to unknown receptors on neuronal cells leading to a dose as well as time-dependent reduction in neuronal cell numbers [1,7]. More studies are needed to identity these unknown receptors.…”

“…Souza et al demonstrated that, AFB1 was capable of modifying the energetic balance associated with ATP metabolism via the inhibition of a crucial enzyme of cellular homeostasis in cells with high as well as moderate energy needs like brain cells [1]. They indicated further that, the inhibition reduces ATP production as well as the interaction sites of ATP initiation and utilization with a resultant inhibition of cerebral sodium-potassium pump (Na + , K + -ATPase) activities [1]. Na + , K + -ATPase is a fundamental enzyme conscientious for the electrochemical gradient across cell membranes, preservation of membrane potential, cell capacity, cellular, as well as excitatory neurotransmitters [1,29].…”

“…They indicated further that, the inhibition reduces ATP production as well as the interaction sites of ATP initiation and utilization with a resultant inhibition of cerebral sodium-potassium pump (Na + , K + -ATPase) activities [1]. Na + , K + -ATPase is a fundamental enzyme conscientious for the electrochemical gradient across cell membranes, preservation of membrane potential, cell capacity, cellular, as well as excitatory neurotransmitters [1,29]. The enzymes required for ATP generation are often perceived at the terminal phase of oxidative phosphorylation (Figure 1) [7].…”

“…Aflatoxins B1(AFB1) is a subsidiary poisonous metabolite archetypally spawned by Aspergillus flavus as well as A. parasiticus [1][2][3]. These species of molds are routinely isolated in warm or tropical counties across the world [1,4]. AFB1 are currently the most ruinous carcinogens amongst all the various kinds of aflatoxins isolated [1,2].…”

“…These species of molds are routinely isolated in warm or tropical counties across the world [1,4]. AFB1 are currently the most ruinous carcinogens amongst all the various kinds of aflatoxins isolated [1,2]. Studies have shown that, ingestion of food contaminated with AFB1 often linked with central nervous system (CNS) disease like neuropathies, demyelinating disease as well as neurocognitive deficits [3,5,6].…”