Abstract
Inositol is a natural substance found widely in plants. It is used in therapies for many medical cases. The aim of this study was to determine the toxicity of myo-inositol (MI) and to investigate its potential hepatoprotective character. In the first part of the study, zebrafish embryos were incubated with 5, 10, 20, 40, 60, 80, and 100 mg/mL MI. Endpoints such as survivability, hatching rate, malformation, and mobility were evaluated. Our results demonstrated that the high doses of MI lead to increased mortality and malformations and reduce the hatching rate in comparison to the control group. Moreover, low doses of this compound do not produce a negative effect on zebrafish and even have the ability to increase the hatching rate and mobility. In the second part of the study, the hepatoprotective effect of MI was tested. Zebrafish larvae from the line Tg (fabp10a:DsRed) were incubated for 24 h with 1% and 2% ethanol (EtOH), 5 mg/mL of MI with 1% EtOH, and 5 mg/mL of MI with 2% EtOH. No significant differences between the groups with EtOH and the group treated with EtOH with MI were observed. Our results suggest that MI has no positive benefits on hepatocytes of zebrafish larvae.
Highlights
Exposure to MI had a significant impact on the hatching of zebrafish larvae (Figure 4)
We examined the liver size, and size, and results that suggested the size in both alcohol concentrations, was significantly results suggested the sizethat in both alcohol concentrations, was significantly lower, even lower, even in groups treated by ethanol solution with
In comparison with the control group, the number of large fat vacuoles in hepatocytes, number of apoptotic cells, necrotic size, stage of liver fibrosis, content of lipid droplets, and inflammatory response were higher in groups treated by TAA. These results showed that in groups of zebrafish treated with TAA and exposed to 0.5 mg/mL Salvia plebeian ethanol extracts (SPEE) for 24 h, all hepatic damage was greatly alleviated
Summary
The human liver is an essential organ that performs a large number of physiological functions. The liver shows the earliest and the greatest degree of tissue injury from excessive drinking because it is the primary site of ethanol metabolism. This contributes to the development of various types of alcoholinduced liver damage [3,4]. As alcohol is broken down in the liver, a number of potentially dangerous products are generated, such as acetaldehyde or free radicals. These products contribute to alcohol-induced liver damage (more than alcohol itself does). The symptoms of liver damage may not appear until the organ’s damage is extensive [2,4]
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