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Death by Sunscreen

Kathy

Well-known member
Not exactly immediate death; but, an association between nanoparticles of a metal element found in some sunscreens and death to brain cells - is nothing to ignore. Note, the infereneces to ROS or reactive oxygen species.

This is the same message which I have been trying to get across on Ranchers for over two years now. Metals interact with proteins. Large and nanoparticle sized metals can react differently within our bodies, eg. cross the blood brain barrier.

Your skin, is another organ of your body, which can absorb these metal contaminates. Please read the News Nature article below. It just came out.

The abstracts below it, regarding manganese and silver nanoparticles, demonstrate that there is more evidence of toxicity involving nanoparticles of metals. I question the practice of seeding clouds with silver nitrate. Did the silver (Ag) form nanoparticles when burned? Has it accumulated in the bioavailable foods which we eat? Mark Purdey found evidence of silver in the horns of CWD afflicted deer and elk in AB/Saskatchewan.

If this doesn't add more evidence to the debate on the harmful effects of Depleted Uranium nanoparticles, I don't know what will.

Do you not agree that far more research needs to be done on the metal connection to protein misfolding?
Link: http://www.nature.com/news/2006/060612/full/060612-14.html

Published online: 16 June 2006; | doi:10.1038/news060612-14

Nanoparticles in sun creams can stress brain cells
Tiny grains send cells into potentially dangerous overdrive.

Tiny particles used in some sun creams have the potential to cause neurological damage, researchers in the United States have found1.

The research does not necessarily imply that these microscopic grains, which are also used in consumer products such as some toothpastes and cosmetics, are harmful in the human body. But it adds to a growing body of evidence that suggests that their safety cannot be taken for granted simply because larger particles of the same substance have no ill effects.

Bellina Veronesi of the US Environmental Protection Agency's research laboratories in North Carolina and her co-workers have studied the effect of nanoparticles of titania (titanium oxide) on cultures of mice cells called microglia, which protect neurons in the brain from harm.

They find that the particles provoke the cells to manufacture chemicals that are protective in the short term but potentially damaging when released in the prolonged manner seen in the experiments.

Günter Oberdörster, a specialist in nanoparticle toxicity at the University of Rochester in New York, stresses that it is too early to say whether the findings reveal a real health hazard. "These are valuable results," he says, "but you have to be very careful about extrapolating them to live organisms."

Into the brain

Nanoparticles are fragments of a material just a few nanometres (millionths of a millimetre) in size. Titania is the white pigment used in paints, and is generally considered non-toxic. It has long been used as a fine powder in many sun creams because of its ability to absorb ultraviolet light.

Some of these creams use titania nanoparticles, which are so small that they appear transparent rather than white. This means that applying the creams on skin does not leave it looking pallid.

The chemicals industry has tended to assume that if large grains are safe, smaller ones will be too. But that assumption is coming under increasing scrutiny, and is not necessarily always valid. "In most cases nanoparticles are unlikely to be dangerous," says Oberdörster, "but we need to look at it on a case-by-case basis."

Scientists working with nanoparticles have known for a long time that size matters: at these very small scales, the properties of materials can change. For one thing, the chemical reactivity of powders depends on their surface area, which increases as the particles get smaller.

But the behaviour of small particles can also be altered by more exotic influences. Quantum-mechanical effects make the colour of light-emitting nanoparticles change with their size, for example.

Nanoparticles may also travel around natural environments, including the human body, in different ways to bigger particles. In particular, they can enter the brain from the bloodstream, whereas big particles cannot. "The blood-brain barrier is normally very tight," says Oberdörster, but nanoparticles can slip through. Many researchers now think that the safety of such particles should be examined as if they were completely new chemicals.

That caution seems to be warranted for titania nanoparticles. Previous studies have suggested that they might be toxic to various types of cell, such as skin, bone and liver cells. Veronesi says that nothing previously was known about their effects on brain cells, however.

Burst or bust?

The researchers used commercially available titania nanopartices about 30 nanometres across, which they added to cultures of mouse microglia. These cells protect neurons in the brain by engulfing foreign particles and releasing a burst of chemicals known as reactive oxygen species (ROS) to 'burn up' the invading substances.

This is a risky strategy, because ROS are also potentially damaging to neighbouring cells. It's a bit like releasing poison gas in a room containing invaders and hoping that it won't seep out into the rest of the building.

Veronesi and colleagues found that titania nanoparticles are swallowed by microglia and that they trigger the release of ROS not as a burst but in a prolonged manner, over an hour or more. That could subject the brain to so-called oxidative stress, which is thought to be the underlying cause of some neurodegenerative diseases such as Parkinson's and Alzheimer's.

It's too early to know how worrying the findings are. No one knows whether nanoparticles applied on the skin, inhaled or ingested can find their way to the brain, or at what concentrations. Effects seen for cultured mice cells might not be duplicated in living mice, let alone in the human body. And there is no firm evidence that this oxidative stress could damage neurons, although Veronesi says they have preliminary results showing that titania nanoparticles can trigger cell death in neurons.

References:
1. Long T.C., et al. Envir. Sci. Technol,
doi: 10.1021/es060589n (2006).


Toxicol Sci. 2006 May 19; [Epub ahead of print]

The Interaction of Manganese Nanoparticles with PC-12 Cells Induces Dopamine Depletion.

Hussain SM, Javorina A, Schrand AM, Duhart H, Ali SF, Schlager JJ.

Applied Biotechnology Branch, Human Effectiveness Directorate, Air Force Research Laboratory, Wright-Patterson AFB, OH.

This investigation was designed to determine whether nano-sized manganese oxide (Mn-40nm) particles would induce dopamine (DA) depletion in a cultured neuronal phenotype, PC-12 cells, similar to free ionic manganese (Mn(2+)). Cells were exposed to Mn-40nm, Mn(2+) (acetate), or known cytotoxic silver nanoparticles (Ag-15nm) for 24 hours. Phase contrast microscopy studies show that Mn-40nm or Mn(2+) exposure did not greatly change morphology of PC-12 cells. However, Ag-15nm and AgNO3 produce cell shrinkage and irregular membrane borders compared to control cells. Further microscopic studies at higher resolution demonstrated that Mn-40nm nanoparticles and agglomerates are effectively internalized by PC-12 cells. Mitochondrial reduction activity, a sensitive measure of particle and metal cytotoxicity, showed only moderate toxicity for Mn-40nm compared to similar Ag-15nm and Mn(2+) doses. Mn-40nm and Mn(2+) dose-dependently depleted dopamine (DA) and its metabolites, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), while Ag-15nm only significantly reduced DA and DOPAC at concentrations of 50 microg/ml. Therefore, the dopamine depletion of Mn-40nm was most similar to Mn(2+), which is known to induce concentration-dependent dopamine depletion. There was a significant increase (>10-fold) in reactive oxygen species (ROS) with Mn-40 nm exposure suggesting that increased ROS levels may participate in dopamine depletion. These results clearly demonstrate that nanoscale manganese can deplete dopamine, DOPAC, and HVA in a dose-dependent manner. Further study is required to evaluate the specific intracellular distribution of Mn-40nm nanoparticles, metal dissolution rates in cells and cellular matrices, if dopamine depletion is induced in vivo, and the propensity of Mn nanoparticles to cross the blood brain barrier or be selectively uptaken by nasal epithelium.

PMID: 16714391


Toxicol Appl Pharmacol. 2005 Jun 15;205(3):271-81. Epub 2004 Dec 8.

Manganese oxidation state mediates toxicity in PC12 cells.

Reaney SH, Smith DR.

Department of Chemistry and Biochemistry, University of California, Santa Cruz, CA 95064, USA. [email protected]

The role of the manganese (Mn) oxidation state on cellular Mn uptake and toxicity is not well understood. Therefore, undifferentiated PC12 cells were exposed to 0-200 microM Mn(II)-chloride or Mn(III)-pyrophosphate for 24 h, after which cellular manganese levels were measured along with measures of cell viability, function, and cytotoxicity (trypan blue exclusion, medium lactate dehydrogenase (LDH), 8-isoprostanes, cellular ATP, dopamine, serotonin, H-ferritin, transferrin receptor (TfR), Mn-superoxide dismutase (MnSOD), and copper-zinc superoxide dismutase (CuZnSOD) protein levels). Exposures to Mn(III) >10 microM produced 2- to 5-fold higher cellular manganese levels than equimolar exposures to Mn(II). Cell viability and ATP levels both decreased at the highest Mn(II) and Mn(III) exposures (150-200 microM), while Mn(III) exposures produced increases in LDH activity at lower exposures (> or =50 microM) than did Mn(II) (200 microM only). Mn(II) reduced cellular dopamine levels more than Mn(III), especially at the highest exposures (50% reduced at 200 microM Mn(II)). In contrast, Mn(III) produced a >70% reduction in cellular serotonin at all exposures compared to Mn(II). Different cellular responses to Mn(II) exposures compared to Mn(III) were also observed for H-ferritin, TfR, and MnSOD protein levels. Notably, these differential effects of Mn(II) versus Mn(III) exposures on cellular toxicity could not simply be accounted for by the different cellular levels of manganese. These results suggest that the oxidation state of manganese exposures plays an important role in mediating manganese cytotoxicity.

PMID: 15922012
 
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