Protective effects of whey on rat liver damage induced by chronic alcohol intake

Abstract

<jats:p> In 2012, alcohol liver disease resulted in 3.3 million—5.9% of global deaths. This study introduced whey protection capacity against chronic alcohol-induced liver injury. Rats were orally administered to 12% ethanol solution in water (ad libitum, average 8.14 g of ethanol/kg body weight (b.w.)/day) alone or combined with whey ( per os, 2 g/kg b.w./day). After 6-week treatment, chronic ethanol consumption induced significant histopathological liver changes: congestion, central vein dilation, hepatic portal vein branch dilation, Kupffer cells hyperplasia, fatty liver changes, and hepatocytes focal necrosis. Ethanol significantly increased liver catalase activity and glutathione reductase protein expression without significant effects on antioxidative enzymes: glutathione peroxidase (GPx), copper–zinc-containing superoxide dismutase (CuZnSOD) and manganese-containing superoxide dismutase (MnSOD). Co-treatment with whey significantly attenuated pathohistological changes induced by ethanol ingestion and increased GSH-Px and nuclear factor kappa B (NF-κB) protein expression. Our results showed positive effects of whey on liver chronically exposed to ethanol, which seem to be associated with NF-κB-GPx signaling. </jats:p>

The effect of ethanol on the mechanisms of liver antioxidant defence – a review of rodent model studies

“…Other authors' experience indicates that acute ethanol intoxication causes a significant increase of catalase activity in liver in both young rats [11] and adult mice [34], contributing to increased oxidation of lipids and proteins in the liver. Prolonged alcohol consumption increases the activity of this enzyme in the liver [35], which is confirmed by the results of experiments by Radic et al [15] using a 12% ethanol solution in rats, and Oh et al [36] using a diet of which 36% of energy value was ethyl alcohol. High alcohol concentration leads to an increase in the reduced form of nicotinamide adenine dinucleotide as a result of the conversion of ethanol to acetaldehyde, and in addition, hydrogen peroxide is formed during ethanol transformation.…”

“…In another experiment, young rats voluntarily consumed 10% ethanol solution for 2, 4 or 6 weeks, which did not affect the SOD activity in the liver [14], as was the case for adult rats receiving 12% ethanol solution for 6 weeks [15]. It can be suspected that the ethanol concentration was too low to cause changes in SOD activity.…”

“…W innym doświadczeniu młode szczury w sposób dobrowolny spożywały 10% roztwór alkoholu etylowego przez 2, 4 lub 6 tygodni, co nie wpłynęło na aktywność SOD w wątrobie [14]. Podobne zjawisko miało miejsce u dorosłych szczurów otrzymujących 12% roztwór etanolu przez 6 tygodni [15]. Można podejrzewać, że stężenie etanolu było zbyt niskie, aby wywołać zmiany w aktywności SOD.…”

“…Długotrwałe spożywanie alkoholu wzmaga aktywność tego enzymu w wątrobie [35], co potwierdzają wyniki doświadczeń zespołu Radic i wsp. [15] (szczury otrzymywały 12% roztwór etanolu), a także Oh i wsp. [36] (alkohol etylowy stanowił 36% wartości energetycznej diety szczurów).…”

“…This study attempts to analyse changes in antioxidant defence parameters based on available literature. There are few experiments in which only the effect of ethanol is analysed as most studies have a broader focus and include the action of other harmful substances like tobacco smoke in combination with exposure to ethanol [17], or the action of substances potentially protecting against, or countering, the effects of exposure to ethanol [15,28,32]. In summary, the consumption of ethanol over a longer period of time contributed to a decrease in the activity of superoxide dismutase (SOD) and glutathione resources, an increase in the activity of glutathione reductase (GR), while in the case of catalase and glutathione peroxidase (GPx), both the increase and decrease of the activity of these enzymes were noted.…”