Protective effects of melatonin and N‐acetylserotonin on aflatoxin B1‐induced lipid peroxidation in rats

Abstract

Aflatoxin B1 (AFB1) is a potent hepatotoxic and hepatocarcinogenic mycotoxin. Reactive oxygen species are considered to participate in the main mechanism of aflatoxin toxicity. Melatonin (Mel) is a hormone which has antioxidative activities. N-acetylserotonin (NAc-5HT) is an immediate precursor of Mel. Melatonin is documented to be completely safe in humans and animals. The aim of our study was to examine the potential protective effects of Mel or NAc-5HT against lipid peroxidation (LPO), caused by AFB1 in male Wistar rats. Mel and NAc-5HT were intraperitoneally (i.p.) injected for 3 weeks in late afternoon (16:00-18:00) injections (20 mg kg(-1) BW/daily). AFB1 (50 microg kg(-1) BW/daily) was administered i.p. 6 h prior to indoleamine injections. Concentrations of malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA), as an index of LPO, were measured in liver, brain, lung, testis and kidney homogenates. The level of LPO in tissue homogenates was expressed as the amount of MDA + 4-HDA (nmol) per milligram of protein. AFB1 increased LPO in the liver, lung, brain and testis, but not the kidney. The increase of LPO caused by AFB1 injections was completely prevented by either Mel or NAc-5HT in all the tissues examined. Melatonin can be considered as a protective pharmacological agent in intoxication with AFB1 and the protective effect of NAc-5HT against aflatoxin-induced LPO broadens the knowledge about its antioxidative properties.

Toxic effect of aflatoxin B1 and the role of recovery on the rat cerebral cortex and hippocampus

“…Second, aflatoxins significantly inhibit acetylcholinesterase activity in the brain and spinal cord which may result in nerve cell degeneration (Cometa et al, 2005). Finally, Aflatoxin administration produces widespread oxidative stress and reduces enzymatic and non-enzymatic antioxidant in the cells with subsequent increase in lipid peroxidation and oxidative DNA damage across the brain (Gesing and Karbownik-Lewinska, 2008;Verma et al, 2007). All these mechanisms disturb cell vital activities and lead to water and ionic shifts which finally cause cell damage and death (Gorun et al, 1978).…”

Protective antioxidative effects of caffeic acid phenethyl ester (CAPE) in the thyroid and the liver are similar to those caused by melatonin

“…In these organs, the antioxidative defence systems are very extensive and comprise both enzymatic and non-enzymatic antioxidants [2,6]. On the other hand, the use of various exogenous antioxidants in both tissues – under condition of increased oxidative stress – has been shown to be beneficial in experimental ( in vitro or in vivo ) studies [2,5,9,10]. Unfortunately, the applicability of different antioxidants in human thyroid or liver diseases has not been yet clearly confirmed in clinical studies and still no effective antioxidative medication is available for widespread use [6-8,10].…”

“…Melatonin (N-acetyl-5-methoxytryptamine), produced in the pineal gland, as well as in numerous other tissues and organs, is a very well-known antioxidant and free radical scavenger, with protective effects against oxidative damage perfectly documented in many tissues, the thyroid and the liver included [9,12-16]. …”

The Effect on Oxidative Stress of Aflatoxin and Protective Effect of Lycopene on Aflatoxin Damage

“…This alteration was associated with a signiicant increase in conjugated diene formation. Concentrations of MDA+ 4-hydroxyalkenals as an index of lipid peroxidation are increased by AFB1 in the liver, lung, brain, and testis, but not the kidney of male Wistar rats [76]. 4-Hydroxynonenal (4-HNE), a major electrophilic by-product of lipid peroxidation caused by oxidative stress, interacts with DNA to form exocyclic guanine products, which have been shown to increase in a rat model of hepatocarcinogenesis.…”