At this point, the processes involving methylmercury moving in an aquatic system have been:
Inorganic mercury deposits in sediments until reaching anoxic regions.
Hg(II) enters microorganisms capable of its methylation and MeHg is released.
It leaves the sediment beds via diffusing towards the water column or aided by some perturbation of the sediments (like bioturbation).
MeHg complexates with (mainly) chloride anions.
This form of MeHg can permeate and partition in cell bodies.
After this, we were kept wondering... if inorganic mercury also permeates and partitions into cells, why is MeHg worst?
Turns out it all depends where in the cell each of the mercury species is fixed. Hg(II) binds better to particulate material (i.e., membranes) whereas MeHg associates with the soluble fraction of the cell. When a higher organism consumes a cell with both Hg(II) and methylmercury, only MeHg will be absorbed because the particulate cellular material is excreted [3]. Thanks (ad)sorption.
This phenomenon is referred to as methylmercury having a greater efficiency of transfer. CH3HgCl continues its journey up the food web thanks to its lipid solubility: it binds to the lipids in fish and other higher animals where it accumulates over time [3]. It is important to mention that most methylmercury in higher animals comes from ingesting methylmercury rich food, rather than the MeHg directly going from the aqueous solution into the animals body.
But! When we reach the fish level in a food web, the amount of methylmercury in muscle tissue is greater than in lipids, meaning that another mechanism -besides MeHg lipid solubility- is involved in the mercury bioaccumulation: affinity of fish intestines to absorb MeHg.