No and Yes!  How is that for an answer?  A somewhat nasty toxicity profile can be traced back through the quinolineconfused pharmacophore all the way back to the cinchona tree (the natural source of the alkaloid compound that the synthetic quinolones had as an inspiration).

The first medical case report of a short-term quinolone induced syndrome from a non-fluorinated quinolone was reported in the year 1972, before fluorinated fluoroquinolones were invented. The report “Nalidixic acid arthralgia” detailed a case of diffuse severe arthralgia, difficulty focusing, photophobia, and CNS disturbances of delirium and hallucinations. Nalidixic acid (trade name NegGram) was the basis for quinolone and fluoroquinolone antibiotics and technically was called a naphthyridine due to the extra nitrogen atom at position eight on the quinolone nucleus, similar to future fluoroquinolones enoxacin, gemifloxacin, tosufloxacin, and trovafloxacin.

Why is fluorine added? Fluorine greatly increases a molecule’s lipophilicity. Incorporating fluorines increases fat solubility, improving its partitioning into membranes and hence increasing bioavailability. In addition fluorine can also aid hydrophobic interactions between the drug and binding sites on receptors or enzymes.

It could be argued that with the addition of fluorine, the subsequent metabolites produced by the FQ molecule’s metabolization, caused an exponential increase in the ability for toxicity.  So, I concede that the fluorine addition probably made a pharmaceutical that had a penchant for toxicity much worse. 

Given that, is it just as simple as detoxing fluoride from our bodies?  Unfortunately no.

Bottom line, the quinolones had the capability to be toxic before the addition of fluorine but gained the ability to be super toxic after the addition of fluorine.