There have been few studies regarding the uptake and risk of environmental organisms. Here, the occurrence of toxic effects was strongly dependent on the type of surface modifications of the nanodiamond. There is currently no study dealing with long-term effects of diamond nanoparticles.

 

One study examined the influence of different surface modifications of nanodiamond particles on the embryonic development of frogs. The frog embryos were exposed to the particles and the development was followed in comparison to untreated embryos. Both the survival and the development of embryonic malformations was strongly dependent on the type of surface modification. The effect spectrum ranged from completely non-toxic (hydroxyl groups on the surface) to highly toxic (carboxyl groups on the surface). For a practical application of the particles thus a non-toxic variant could be selected [1].

 

The nematode C. elegans, which usually feeds on bacteria ingests diamond nanoparticles and enriches it in the gut. A transition from unmodified particles from the gut into the body tissue does not occur, however, dextran and albumin-coated particles are able to pass through the intestinal mucosa [2]. Despite these differences in the absorption none of the particles used is toxic to the nematodes. Lifetime, number of offspring, ROS level as well as stress response does not differ from untreated control worms.

 

In contrast, nanodiamond influenced reproduction and survival in water fleas. First, it was found microscopically that the particles adhere to the exoskeleton of the animals and also accumulate in the intestines. The latter can lead to decreased absorption of nutrients, leading to increased mortality (from 12,5 mg/l) and subsequently to a reduction in the reproductive rate (from 1,3 mg/l) [3]. An uptake of the particles from the intestine into the body's cells was not observed.

 

 

Literatur arrow down

  1. Marcon, L et al. (2010), J Mater Chem, 20(37): 8064-8069.
  2. Mohan, N et al. (2010), Nano Lett, 10(9): 3692-3699.
  3. Mendonca, E et al. (2011), J Hazard Mater, 186(1): 265-271.

 

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