ß-Carotene Supplementation Improves Pancreas Function during Moderate Ethanol Consumption: Initial Characterization from a Morphological Overview.

Alcohol is believed to harm acinar cells, pancreatic ductal epithelium, and pancreatic stellate cells. After giving ethanol and/or ß-carotene to C57BL/6 mice, our goal was to evaluate their biochemistry, histology, and morpho-quantitative features. There were six groups of C57BL/6 mice: 1. Group C (control), 2. Group LA (low-dose alcohol), 3. Group MA (moderate-dose alcohol), 4. Group B (ß-carotene), 5. Group LA + B (low-dose alcohol combined with ß-carotene), and 6. Group MA + B (moderate-dose alcohol combined with ß-carotene). After the animals were euthanized on day 28, each specimen's pancreatic tissue was taken. Lipase, uric acid, and amylase were assessed using biochemical assessment. Furthermore, the examination of the pancreatic structure was conducted using Ammann's fibrosis scoring system. Finally, the morpho-quantitative characteristics of the pancreatic islets and acinar cells were determined. In the serum of the MA + B group, there were higher amounts of total amylase (825.953 ± 193.412 U/L) and lower amounts of lipase (47.139 ± 6.099 U/L) (p < 0.05). Furthermore, Ammann's fibrosis punctuation in the pancreas revealed significant variations between the groups (p < 0.001). Finally, the stereological analysis of pancreatic islets showed that the groups were different (p < 0.001). These findings suggest that antioxidant treatments might help decrease the negative effects of ethanol exposure in animal models.

ß-Carotene Increases Activity of Cytochrome P450 2E1 during Ethanol Consumption.

One of the key routes through which ethanol induces oxidative stress appears to be the activation of cytochrome P450 2E1 at different levels of ethanol intake. Our aim was to determine if oral ß-carotene intake had an antioxidant effect on CYP2E1 gene expression in mice that had previously consumed ethanol. C57BL/6 mice were used and distributed into: control (C), low-dose alcohol (LA), moderate-dose alcohol (MA), ß-carotene (B), low-dose alcohol+ß-carotene (LA + B), and moderate-dose alcohol+ß-carotene (MA + B). Animals were euthanized at the end of the experiment, and liver tissue was taken from each one. CYP2E1 was measured using qPCR to detect liver damage. The relative expression level of each RNA was estimated using the comparative threshold cycle (Ct) technique (2-ΔΔCT method) by averaging the Ct values from three replicates. The LA+B (2267 ± 0.707) and MA+B (2.307 ± 0.384) groups had the highest CYP2E1 fold change values. On the other hand, the C (1.053 ± 0.292) and LA (1.240 ± 0.163) groups had the lowest levels. These results suggest that ethanol feeding produced a fold increase in CYP2E1 protein in mice as compared to the control group. Increased CYP2E1 activity was found to support the hypothesis that ß-carotene might be dangerous during ethanol exposure in animal models. Our findings imply that ß-carotene can increase the hepatic damage caused by low and high doses of alcohol. Therefore, the quantity of alcohol ingested, the exposure period, the regulatory mechanisms of alcoholic liver damage, and the signaling pathways involved in the consumption of both alcohol and antioxidant must all be considered.

Differential expression of µ-opioid receptors in the nucleus accumbens, amygdala and VTA depends on liking for alcohol, chronic alcohol intake and estradiol treatment.

Affectations of the opioid system have been related to exacerbated alcohol consumption. The objectives of this work were to assess whether a deficit of ß-endorphinergic neurons differentially affects alcohol intake in female rats with low (LC) and high alcohol consumption (HC), and to determine changes in the µ-opioid receptors (MOR) related to alcohol consumption and chronic exposure to alcohol in structures of the mesolimbic system. Female wild-type rats were selected according to their baseline alcohol intake levels and then exposed to chronic voluntary alcohol consumption after a single injection of either the vehicle or estradiol valerate (EV) to produce a ß-endorphin neuronal deficit. Changes in alcohol consumption and MOR expression levels were assessed in the nucleus accumbens (NAc), amygdala (Amy) and ventral tegmental area (VTA) at 5 and 10 weeks after EV treatment. The LC rats increased alcohol intake from baseline to the initial weeks after EV treatment and this consumption remained stable throughout the studied period. In contrast, alcohol consumption increased steadily over time in the HC rats. The HC vehicle rats had a 38% higher MOR protein expression in the NAc than the LC vehicle rats. In addition, chronic alcohol consumption increased MOR expression in the Amy regardless of consumption level, whereas EV treatment produced a decrease in MOR expression in the VTA in all groups. These results suggest intrinsic differences in MOR expression related to alcohol consumption levels. Also, the EV treatment and chronic exposure to alcohol produced adaptive changes in MOR expression.