Pesticides, Herbicides and Mitochondrial Disease

Last night, a friend who lives just a few neighborhoods over from us, sent me an email letting me know that her neighborhood was getting ready to spray this week using a product called SPEEDZONE. This is not the first time I have heard of SPEEDZONE. Last fall this same friend had alerted me (due to her concerns over the safety of it for her children and her family) and I did some research on its toxic side effects. At that time, I wrote her community’s landscape committee and voiced my concerns as a neighbor who is also affected by what communities outside of my own, do- based on breathing the same air and drinking the same water and playing at the same parks that these herbicides come in contact with. So when this came across my computer screen again last night… I decided to do some more digging…and WHOA…what a can of worms I un-earthed… not just about this pesticide/herbicide but many other common ones used, as well :


Interactions of herbicides 2,4-D and dinoseb with liver mitochondrial bioenergetics.

Environmental and Occupational Medicine book

2,4-D Toxicity: Cause, Effect and Control

The herbicide has low to moderate acute toxicity towards humans and animals, but some results suggest a chronicle and/or genotoxic metabolic disturbances.

Mechanisms of toxicity, clinical features, and management of acute chlorophenoxy herbicide poisoning: a review.

Mitochondria-Mediated Cell Injury

Paraquat and 2,4-D caused a dose- and time-dependent cell death (Fig. 4) accompanied by depletion of intracellular reduced glutathione (GSH) and a corresponding increase in oxidized glutathione (GSSG) (Palmeira et al., 1994a).

The correlations of decreased GSH are also very high for paraquat and 2,4-D, suggesting the decreased GSH/GSSG ratio is involved in the induction of irreversible cell injury.


Comparative effects of the Roundup and glyphosate on mitochondrial oxidative phosphorylation

Therefore, the uncoupling of oxidative phosphorylation is also related to the non-specific membrane permeabilization induced by Roundup.

Bearing in mind that mitochondria is provided with a variety of bioenergetic functions mandatory for the regulation of intracellular aerobic energy production and electrolyte homeostasis, these results question the safety of Roundup on animal health.

Glyphosate Formulations Induce Apoptosis and Necrosis in Human Umbilical, Embryonic, and Placental Cells

This work clearly confirms that the adjuvants in Roundup formulations are not inert. Moreover, the proprietary mixtures available on the market could cause cell damage and even death around residual levels to be expected, especially in food and feed derived from R formulation-treated crops.

Effect of pesticides on cell survival in liver and brain rat tissues.

The treatment of Wistar rats with the pesticides (i.p. 1/250 LD50, three times a week for 5 weeks) caused loss of mitochondrial transmembrane potential and cardiolipin content, especially in substantia nigra (SN), with a concomitant increase of fatty acid peroxidation.

Mitochondrial Depletion and Round Up

Birth Defects and Round Up


I first Learned of Rotenone from Dr. Bruce Cohen’s video (below). Dr. Cohen is one of the experts in mitochondrial disease and practices at Akron Children’s Hospital in Ohio. (see 2:40 for a discussion about Toxins and Rotenone):

The rotenone model of Parkinson’s disease: genes, environment and mitochondria

Parkinson’s disease (PD) is occasionally caused by single gene mutations or by single toxic exposures, but most cases of PD are probably caused by some combination of genetic susceptibility and environmental exposure. Using rotenone as a prototype for an environmental toxicant, we argue here that genetic and environmental causes of PD converge on common pathogenic mechanisms. If so, protective strategies devised for one type of PD may be broadly useful for other forms of the disease.

Mitochondrial Function and Dysfunction


Now if you ask me if I believe pesticides/herbicides are the single solitary cause of mitochondrial disease, I will tell you no. But I do believe that this is a PRIME example of where genetics and environment interplay. I do believe there are individuals who have a genetic disposition to be more sensitive to certain substances…whether those be foods, naturally occurring chemicals, man-made chemicals, pharmaceuticals, etc.  And for those genetically predisposed individuals who may already have altered mitochondrial energy production, then substances that further attack and degrade the mitochondrial’s ability to produce energy could feasibly make a person’s condition worse. Really, if you think about it, it is no different from an asthmatic avoiding a room full of smoke (or wildfire filled air in TX) or a child with an anaphylactic PEANUT allergy avoiding Texas Roadhouse for dinner (where buckets of un-shelled peanuts line the walls and the floor is covered in peanut shells!). AVOID that which brings you HARM… plain and simple. One more reason to buy Organic or Grow your own, if you can! And if you can’t AVOID what brings you harm, because it is being sprayed all around you without your consent or knowledge sometimes, then SPEAK UP and make your voice heard. KATY, TEXAS Neighbors can start here:

About Empowered Advocacy Pediatric Patient Advocate
This entry was posted in ADHD, Allergies, Asthma, Autism, Medical, Mitochondrial Disease, Pesticides. Bookmark the permalink.

4 Responses to Pesticides, Herbicides and Mitochondrial Disease

  1. Jenna says:

    Wow… that was crazy to see. I would like to see that documentary. I didn’t see it on netflix. I will look into where I can see it. The way you feel about mito and the environment is the way I feel about autism and vaccines.

  2. Pingback: Autism PREVENTION Part 2: Mitochondrial Toxin Exposure | Taking Baby{food}Steps…

  3. Anonymous says:

    I think it is to me that the use of these toxins should be outlawed. Ddt is no longer available. And we have survived so we will get along fine without the rest of the toxins later Sheppard

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