Is ethanol harmful for the human body?
Exposure to high concentrations of ethanol vapours may cause irritation of the eyes, skin and respiratory tract, loss of coordination (ataxia), sleepiness, narcosis (stupor or unconsciousness), impaired perception and lack of coordination. Low ethanol improves insulin resistance, increases high-density lipoprotein and stimulates activity of the antioxidant enzyme, paraoxonase. In conclusion, we suggest that chronic low ethanol intake confers its beneficial effect mainly through its ability to increase antioxidant capacity and lower AGEs.In general, ethanol causes oxidative stress-related damage in the kidneys, but sometimes, in some conditions, it also improves the antioxidant capacity of the renal cells. Unfortunately, we only know that low-concentration ethanol can improve renal antioxidant capacity, but the exact dose and period are still unclear.
What are the dangers of ethanol?
Ingesting ethanol can cause mood changes, slower reaction time, uncoordinated movements, slurred speech and nausea. Higher exposures may cause blurred vision, confusion and disorientation, movement problems, vomiting and sweating. Severe effects include double vision, coma, low temperature and fitting. Ethanol alters learning and memory (Oslin and Cary, 2003; White, 2003), and this may involve effects on synaptic plasticity, including long-term depression (LTD) and long-term potentiation (LTP) (reviewed in Zorumski et al.A clinically prominent acute action of ethanol is to suppress anxiety. In experimental animals, ethanol potentiates GABA-ergic transmission [1], and reduces experimental anxiety 4, 26, 41.
Is ethanol bad for your liver?
The majority of ethanol metabolism occurs in the liver. Consequently, this organ sustains the greatest damage from ethanol abuse. Ethanol consumption disturbs the delicate balance of protein homeostasis in the liver, causing intracellular protein accumulation due to a disruption of hepatic protein catabolism. Alcohol induces fatty liver by increasing the ratio of reduced form of nicotinamide adenine dinucleotide to oxidized form of nicotinamide adenine dinucleotide in hepatocytes; increasing hepatic sterol regulatory element-binding protein (SREBP)-1, plasminogen activator inhibitor (PAI)-1, and early growth response-1 .