Gentamicin is an unusual antiobiotic with two properties that make it particularly useful in plant cell culture: it is autoclavable so is added to media before autoclaving/sterilization, and it is active against mycoplasmas as well as gram positive and gram negative bacteria. Over the last week, I too have been getting it. I discovered this way other unusual properties: while nearly any other drug is metabolized in the body, gentamicin is excreted unchanged. There is also much more than the usual fuss in prescribing it: careful does correlation of ‘lean body weight’ against dose (7mg/kg up to 640mg max daily) , and blood testing after the first dose to check the excretion rate: it will bind to many molecules so travels slowly out of the system. It is given intravenously, diluted in c. 100ml of 0.9% saline, as it is not absorbed orally, so is a drug restricted to hospitals.
It is isolated from the gram-positive aerobic and mycelial soil bacterium Micromonospora purpurea and was discovered in 1963. Despite both the name of the antibiotic and species from which gentamicin is isolated, it is a white powder or clear solution. Why is it spelt ‘-micin’ rather than the ‘-mycin’ of products from other mycelial bacteria and fungi? It seems that aminoglycoside antibiotics from this genus end with -micin, to distinguish them from those from those isolated from Streptomyces with different taxonomic affinities (e.g. neomycin and streptomycin).
Gentamicin shares some properties with another antibiotic widely used in plant research, kanamycin: both are aminoglycosides and work partly by interaction with the 30S subunit of prokaryotic ribosomes, inhibiting prokaryotic protein synthesis. However, the two antibiotics act independently, and there are resistance genes which confer resistance only to gentamicin. The 30S inhibition means these are two of the antibiotics active against mycoplasmas (http://www.sigmaaldrich.com/life-science/core-bioreagents/learning-center/antibiotic-selection.html). Interestingly, Micromonospora seems to gain resistance to its own antibiotic through methylation of 16S ribosomal RNA (rRNA) in the 30s ribosomes. Although resistance among other bacteria is rare, this methylation has recently appeared as a mechanism of resistance against aminoglycosides among gram-negative pathogens; given the therapeutic use still, perhaps gentamicin resistance is not the ideal selectable marker to use in plasmids.