Great question.

First, I would suggest this paradigm: Ethanol toxicity manifests primarily from ROS build up downstream of hepatic inability to process aldehyde fast enough. Protective agents would feature those most able to ramp up the ARE system. Nrf2 activators would figure highly. Sulforaphane is the canonical example. A wide range of polyphenols convey benefit, including anthocyanin.

Resveratrol and curcumin are examples that hit additional pathways involving autophagy and inflammatory reduction. Some of these compounds compete with alcohol and aldehyde to some degree for catabolism. AMPK stimulation is another pathway. Any senolytics, also, is likely to help.

Ethanol itself causes very few problems compared to aldehyde. Ethanol ---(alcohol dehydrogenase)--> Acetaldehyde ---> (acetaldehyde dehydrogenase) --> Acetate. Protective agents would be those that inhibit alcohol dehydrogenase while increasing the activity of acetaldehyde dehydrogenase.

General re polyphenols

Article Protective Role of Polyphenols against Vascular Inflammation...

Plenty of specific articles.

Ex: Article Effect of Mixed Fruit and Vegetable Juice on Alcohol Hangove...

Here's many:

https://www.ncbi.nlm.nih.gov/pubmed/?term=hangover%5Btitle%5D

I have not seen the melatonin aspect but acute ethanol ingestion enhances brain Casp-3 activity (apoptosis), HoCys and S-adenosylhomocysteine levels, which are sufficient to cause considerable damage. Let me know if you want to discuss, I have unpublished data from animal models.