Well I am glad that Roger Morton seems to understand some of Mae Wan Ho's
dribble but I have no idea what she means. Is this perhaps a joke? I would
love to counter her claims but I can't figure out what they are. What has
the second law of thermodynamics got to do with anything? It is a simple
statement about the the fact that there is a general tendency towards
disorder in the Universe.
This is less than first year physics. I learnt this stuff in High School.
Obviously life avoids degeneration by eating. Perhaps Mae Wan Ho derives
her energy from crystals or something. Even eating won't be enough in the
end because, as most of us know, the only sure thing after birth is death.
I suggest a simple experiment for her, followed by an explanation (like a
high school lab report). Heat a beaker of water using a bunsen burner and
explain why the water gets hot and why it cools down after the energy
source is removed.
I suspect that I am being slightly cruel here because I can't believe that
she is serious. I am inclined not to read this nonsense or reply to it but
I am still puzzled as to why there is a University in the UK that employs
"biologists" who are bordering on the insane. It is probably best not
reply to these kind of slightly left of loony diatribes because it only
the views expressed here are entirely my own and no way reflect those of
my employer (except that even they have to admit that this is unreal)
Subj: Re: Mae-Wan Ho's Research
From: "Gordon Couger"
>"But as there need be no entropy generated in adiabatic processes - which
occur frequently in living systems (see below) - the division into
available and nonavailable energy cannot be absolute"
> Am I mistaken, or does Dr Ho claim to have discovered a situation where
the second law of thermodynamics is broken?
If this is truly the case the problem of nitrogen balance for organic
farming is solved. The just use the BS they are spouting for fertilizer.
I can have respect for a person that has ethical, moral or scientific
differences of opinion but when they don't understand the basic laws of
science and try to BS their way through they belong in politics not
Gordon Couger email@example.com
Retired Farmer www.couger.com/gcouger
Subj: RE: Toxic Pollen ?
From:"KAUFMANN, JOHN E [AG/FDPD]"
Please tell me with all the allergic reactions people have to pollen, to
the extent that we have pollen counts listed along with the weather at
certain times of the year, how Thomas Lovejoy can say "There is no
previous reference to pollen being toxic."
From: AgBioView [mailto:AgBioViewfirstname.lastname@example.org] GM Food Debate Gets
Spicy: Recalled taco shells with engineered corn fuel controversy
Subj: Re: genetic stability
From: David Hildebrand
Its been said that genetic engineering of plants promotes genetic
instability by for example stimulating movement of transposons. Its my
understanding that long tissue culture/hormone treatment can stimulate
this but does anyone know if there is any evidence that gene transfer per
se might promote movement of mobile genetic elements?
David Hildebrand, Professor Dept. Agronomy Univ. Kentucky
Subj: Rotenone backgrounder
From: Shane Morris
Backgrounder: Rotenone and Parkinson's Disease by Shane Morris and Doug
Powell, Centre for Safe Food, University of Guelph
Article URL: http://www.plant.uoguelph.ca/safefood/chem-haz/rotenone.htm
Two papers to be published in the Dec. 2000 issue of Nature Neuroscience
and presented at a conference yesterday have raised questions about links
between the so-called natural pesticide, rotenone, and Parkinson's disease.
The papers in question are:
Ranjita Betarbet, Todd B. Sherer, Gillian MacKenzie, Monica Garcia-Osuna,
Alexander V. Panov and J. Timothy Greenamyre. (2000) Chronic systemic
pesticide exposure reproduces features of Parkinson's disease. Nature
Neuroscience, Vol. 3, p 1301.
Benoit I. Giasson and Virginia M.-Y. Lee. (2000) A new link between
pesticides and Parkinson's disease, Nature Neuroscience, Vol. 3, p 1227
Rotenone is a so-called natural pesticide that has a variety of known and
speculated biological effects. Although not widely used by organic
growers, rotenone is found in a variety of commercial garden and
animal-care products. This latest research underscores the need for
specific end-product safety and environment risk assessments, irrespective
of process or origin.
Rotenone has been marketed as an organic pesticide (home and commercial
use), piscicide (fish toxin) and as an active ingredient for lice and tick
control on pets in for several decades. It is often commercially
formulated as dusts, powders, and sprays (less than 5% active ingredient)
for use in gardens and on food crops. Trade names for products containing
rotenone include Chem-Fish, Cuberol, Fish Tox, Sinid and Tox-R Noxfish,
Noxfire, Rotacide, Foliafume, Nusyn-Noxfish, PB-Nox, Prentox, Chem-Fish,
Rotenone Solution FK-11. It is also marketed as Curex Flea Duster, Derrin,
Cenol Garden Dust, Chem-Mite, Cibe Extract and Green Cross Warble Powder.
The compound may also be used in formulations with other pesticides such
as carbaryl, lindane, thiram, piperonyl butoxide, pyrethrins and quassia.
Rotenone is derived from the root of various plants of the Derris or
Lonchocarpus species from Southeast Asia, Central and South America, and
can be found in at least 68 species of Legumes. It is available in at
least 300 formulated products from a large number of manufacturers and is
often made more efficacious by the addition of piperonyl butoxide (PBO),
which is another botanical material. Rotenone is expensive compared with
synthetic insecticides, but is moderately priced for a botanical. It is
the most commonly mentioned of the botanicals in pre-synthetic literature,
and is at least somewhat effective against a large number of insect pests.
These include: pear psylla, strawberry leafroller, European corn borer,
European apple sawfly, cherry fruit fly, apple maggot, cranberry
fruitworm, raspberry fruitworm, pea aphid (which is similar to rosy apple
aphid), European red mite and two-spotted spider mite, codling moth, plum
curculio, Japanese beetle and tarnished plant bug. Rotenone is toxic to
ladybird beetles and predatory mites, but non-toxic to syrphid flies that
feed on aphids, and to honeybees. Rotenone is rapidly degraded by
sunlight, lasting a week or less.
There is evidence of very early usage, as in 1649 it was reported to be
used in South America to paralyze fish, which were then netted. In 1848 in
Asia, rotenone was cited as used as an insecticide to control leaf eating
Mode of action: Rotenone is a cell respiratory enzyme inhibitor (it acts
as a stomach poison in insects (Fields et al, 1991)). Its ultimate
mode-of-action involves disruption of cellular metabolism, acting between
NAD+ (a coenzyme involved in oxidation and reduction in metabolic
pathways) and coenzyme Q (a respiratory enzyme responsible for carrying
electrons in some electron transport chains), resulting in failure of the
respiratory functions (Ware, 2000). Essentially, Rotenone inhibits a
biochemical process at the cellular level making it impossible for the
target organism to use oxygen in the release of energy needed for body
processes and hence blocks conduction of nerve impulses
Rotenone is a "steroid shaped" molecule that kills insects and it has been
used as a fish poison.
CAS Number: 83-79-4
Molecular Weight: 394.43
Water Solubility: 15 mg/L @ 100 C, slightly soluble in water Solubility in
Other Solvents: s. in acetone, carbon disulfide and chloroform; s.s in
alcohols and carbon tetrachloride Melting Point: 163 C
Vapor Pressure: <1 mPa @ 20 C
Partition Coefficient: Not Available
Formulations include crystalline preparations (approximately 95% pure),
emulsified solutions (approximately 50% pure), and dusts (approximately
0.75 to 5% pure). This profile refers to the crystalline preparation
unless otherwise noted. (SEE APPENDIX I)
Rotenone and Parkinson studies:
The link between Rotenoone has been suspected for several years. In this
regard some of the leading work is summarized below. When rotenone has
been injected into animals, tremors, vomiting, inco-ordination,
convulsions, and respiratory arrest have been observed. These effects have
not been reported in occupationally exposed humans
Postmortem studies and animal models strongly implicate mitochondrial
impairment in the pathogenesis of Parkinson's disease.
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), an inhibitor of the
mitochondrial electron transfer chain, induces Parkinsonism in
experimental animals and in humans after inadvertent ingestion. Chronic
exposure to rotenone, a common pesticide and potent inhibitor of the
electron transfer chain, also produces selective nigrostriatal
degeneration and cytoplasmic inclusions reminiscent of Lewy bodies.
Mitochondrial dysfunction has numerous consequences, including energetic
failure, generation of reactive oxygen species, disregulation of calcium
homeostasis and induction of apoptosis, each of which may be important in
Parkinson's disease. Secondary consequences of mitochondrial dysfunction
may include oxidative damage to cellular components and abnormal protein
aggregation. Thus, there is a compelling need to elucidate the role of
mitochondrial defects in Parkinson's disease, to define the mechanisms by
which mitochondrial impairment kills neurons, and to identify therapeutic
strategies to prevent the cell death that accompanies mitochondrial
Complex I dysfunction has been implicated in the pathogenesis of
Parkinson's disease and in the neurotoxicity of
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which produces a
Parkinsonian syndrome in experimental animals and humans. Rotenone is an
insecticide has been known for several years as a specific inhibitor of
In particular it has been known since 1997 that systemic administration of
rotenone produces selective damage in the striatum and globus pallidus,
but not in the substantia nigra. (Ferrante et al, Brain Res 1997 Apr.
4;753(1):157-62). In this specific study the scientists examined the
pattern of central nervous system damage produced by i.v. systemic
administration of rotenone in rats. Rotenone produced selective damage in
the striatum and the globus pallidus, but the substantia nigra was spared.
These results are consistent with prior reports suggesting that the
selective vulnerability of the substantia nigra to MPTP involves both
uptake by the dopamine transporter as well as complex I inhibition, and
they show that rotenone produces a unique pattern of central nervous
In 1999, another study (Greenamyre et al, 1999) knowing that the reduced
activity of complex I of the electron-transport chain had been implicated
in the pathogenesis of both mitochondrial permeability transition
pore-induced Parkinsonism and idiopathic Parkinson's Disease, developed a
novel model of the disease. Using this model it was shown that chronic,
systemic infusion of rotenone, a complex-I inhibitor, selectively killed
terminals and caused retrograde degeneration of substantia nigra neurons
over a period of months.
Again in late 1999, M. Friedrich wrote a piece entitled "Rotenone study
aids Parkinson research"
(Friedrich, 1999 or
http://www.ext.usu.edu/publica/agpubs/pestic/newslet/dec99.htm) in which
he described an experimental model which appeared to reproduce the
neurochemical, neuropathological, and behavioral features of the disease
through chronically exposing laboratory rats to the pesticide rotenone. He
further explained that the protocol for the model was simple, the goal
being to use low dosages (of rotenone) for long periods of time. He wrote
"male rats were given rotenone by continuous infusion via minipumps for
anywhere from 2 days to 3 months. The animals became progressively slower
in movements and reflexes and more rigid. The results of the investigation
indicate that systemic administration of rotenone brings about selective
retrograde degeneration and mimics the slowly progressive course of
Parkinson Disease. Systemic rotenone infusion may provide an accurate
model for the continuously progressive, chronic degeneration that
characterizes the disease and may provide a novel and more accurate model
to study neuroprotective drugs."
Earlier this year, knowing from a previous study, that rotenone, a complex
I inhibitor, induced a rapid accumulation of DOPAL and DOPET in the medium
of cultured PC12 cells an experiment was done that showed results
indicating that accumulation of DOPAL was responsible for the potentiated
rotenone-induced toxicity following combined inhibition of ALDH and ARs.
Since complex I dysfunction is reported to be involved in the pathogenesis
of Parkinson's disease, DOPAL potentiation of the deleterious effects of
complex I inhibition may contribute to the specific vulnerability of
dopaminergic neurons to injury. (Lamensdorf et al, 2000)
Regulatory Commercial Notes:
In the U.S., 10 rotenone products were withdrawn or canceled at the
request of the registrants in 1999. The products can be sold for another
year, and end-users can continue to use the pesticides according to the
label (which has been voluntarily canceled for food uses). In1997, AgrEvo
-- due to the high cost of re-registration -- deleted from their label the
usage on domestic pets. (FR Vol. 61, 12-3-96).
Fields, P.G Arnason, J.T., Philogene B.J., Aucoin R.R, Morand P.,
Soucy-Breau C.(1991) Phototoxins as Insecticides and Natural Plant
Defenses. Mem. ent. Soc. Can . IS9: 29-38
Friedrich M. (1999) Rotenone study aids Parkinson research, JAMA Dec
Greenamyre JT, MacKenzie G, Peng TI, Stephans SE (1999) Mitochondrial
dysfunction in Parkinson's disease.
Biochem Soc Symp 1999;66:85-97
Lamensdorf I, Eisenhofer G, Harvey-White J, Nechustan A, Kirk K, Kopin IJ
(2000) 3,4 Dihydroxyphenylacetaldehyde potentiates the toxic effects of
metabolic stress in PC12 cells. Brain Res Jun 23;868(2):191-201
Ware G.W. (2000) AN INTRODUCTION TO INSECTICIDES (3rd Edition) In E. B.
Radcliffe and W. D. Hutchison [eds.], Radcliffe's IPM World Textbook, URL:
Added Notes on General Toxicity:
When compared to most botanicals, rotenone is the most toxic to humans and
other mammals. The acute oral LD50 is from 601500 mg/kg. In small doses it
may be irritating or numbing to mucous membranes.
Acute toxicity: Local effects on the body include conjunctivitis,
dermatitis, sore throat, and congestion. Ingestion produces effects
ranging from mild irritation to vomiting. Inhalation of high doses can
cause increased respiration followed by depression and convulsions. The
compound can cause a mild rash in humans and is a strong eye irritant to
rabbits. The oral LD50 of rotenone ranges from 132 to 1500 mg/kg in rats.
The reported LD50 of rotenone in white mice is 350 mg/kg. A spray of 5%
rotenone in water was fatal to a 100-pound pig when exposed to 250 cubic
centimeters (mL) of the airborne mixture. In rats and dogs exposed to
rotenone in dust form, the inhalation fatal dose was uniformly smaller
than the oral fatal dose. Rotenone is believed to be moderately toxic to
humans with an oral lethal dose estimated from 300 to 500 mg/kg. Human
fatalities are rare, perhaps because rotenone is usually sold in low
concentrations (1 to 5% formulation) and because its irritating action
causes prompt vomiting. The mean particle size of the powder determines
the inhalation toxicity. Rotenone may be more toxic when inhaled than when
ingested, especially if the mean particle size is very small and particles
can enter the deep regions of the lungs.
Chronic toxicity: Growth retardation and vomiting resulted from chronic
exposures of rats and dogs. Rats fed diets containing rotenone at doses up
to 2.5 mg/kg for 2 years developed no pathological changes that could be
attributed to rotenone. Dogs fed doses of rotenone up to 50 mg/kg/day for
28 days experienced vomiting and excessive salivation, but no decreased
weight gain. Dogs fed rotenone for six months at doses up to 10 mg/kg/day
had reduced food consumption and therefore reduced weight gain. At the
highest dose, blood chemistry was adversely affected, possibly due to
gastointestinal lesions and chronic bleeding. Examination of 35 tissue
types revealed only one type of lesion that might have been associated
with exposure to the test chemical: lesions of the GI tract.
Reproductive effects: Pregnant rats fed 10 mg/kg/day on days 6 through 15
of gestation experienced decreased fecundity, increased fetal resorption,
and lower birthweight. Very high maternal mortality was seen at this dose.
The 2.5 mg/kg/day dose produced no observable maternal toxicity or adverse
effect on fetal development. Fetotoxicity and failure of offspring are
reported in guinea pigs at doses of 4.5 and 9.0 mg/kg/day for an
unspecified period. Thus reproductive effects seem unlikely in humans at
expected exposures. Teratogenic effects: Pregnant rats fed 5 mg/kg/day
produced a significant number of young with skeletal deformities. The
effects were not observed at the 10 mg/kg/day level, so the data do not
provide convincing evidence of teratogenicity because the effects do not
appear to be dose-related. Thus, the evidence for teratogenicity is
inconclusive. Mutagenic effects: The compound was determined to be
nonmutagenic to bacteria and yeast and in treated mice and rats. However,
it was shown to
cause mutations in some cultured mouse cells. In summary, the data
regarding the mutagenicity of rotenone are inclusive.
Carcinogenic effects: Studies in rats and hamsters have provided limited
evidence for carcinogenic activity of rotenone. No evidence of
carcinogenic activity was seen in hamsters at oral doses as high as 120
mg/kg/day for a period of 18 months. Studies of two species of rats
evidenced no statistically significant cancerous changes in any organ
site, including mammary glands, at oral doses of up to 75 mg/kg/day for 18
months. Significant increases in mammary tumors have been reported in
albino rats with intraperitoneal doses of 1.7 mg/kg/day for 42 days, and
in Wistar rats at approximately 1.5 mg/kg/day orally for 8 to 12 months.
In the latter study, however, higher dose rates (3.75 and 7.5 mg/kg/day)
over the same period did not produce increased tumors. Thus, the evidence
for carcinogenicity is inconclusive.
Organ toxicity: Chronic exposure may produce changes in the liver and
kidneys as indicated by the animal studies cited above.
Fate in humans and animals: Absorption in the stomach and intestines is
relatively slow and incomplete, although fats and oils promote its uptake.
The liver breaks down the compound fairly effectively . Animal studies
indicate that possible metabolites are carbon dioxide and a more
water-soluble compound that can be excreted in the urine. Studies
indicated that approximately 20% of the applied oral dose (and probably
most of the absorbed dose) may be eliminated from animal systems within 24
hours. Related symptomatic occupational exposures in humans involving
flea-control dips were identified. Responsible active ingredients were
rotenone/pyrethrin (five cases); rotenone, (one case ). Eight workers
developed moderate health effects that required some form of treatment,
and 18 developed minor health effects (minimally bothersome symptoms that
resolved rapidly). Among the workers with moderate health effects two were
cased by rotenone/pyrethrin
Effects on birds: Rotenone is slightly toxic to wildfowl. The LD50 values
for rotenone in mallards and pheasants are (greater than) 2000 mg/kg and
1680 mg/kg respectively. A dietary LC50 of 4500 to 7000 ppm is reported in
Effects on aquatic organisms: Since rotenone is used as a fish toxin
(piscicide), it follows that it is very highly toxic to fish. Reported
96-hour LC50s were 0.031 mg/L in rainbow trout, 0.0026 mg/L in channel
catfish, and 0.023 mg/L in bluegill for the 44% pure formulation. Aquatic
invertebrates have a wide range of sensitivity to rotenone with 48-hour
EC50 values ranging from 0.002 to 100 mg/L. The compound is not expected
to accumulate appreciably in aquatic organisms. The bioconcentration
factor for rotenone in the sunfish is 181 times the ambient water
concentration. In addition the highly toxic nature of this substance to
aquatic organisms means that there is little survival of the organisms
that accumulate the compound.
Effects on other organisms: The compound is nontoxic to bees. However, it
is toxic to bees when used in combination with pyrethrum.
Breakdown in soil and groundwater: Rotenone is rapidly broken down in soil
and in water. The half-life in both of these environments is between 1 and
3 days. It does not readily leach from soil, and it is not expected to be
a groundwater pollutant. Rotenone breaks down readily by exposure to
sunlight. Nearly all of the toxicity of the compound is lost in 5 to 6
days of spring sunlight or 2 to 3 days of summer sunlight. Breakdown in
water: Rotenone is rapidly broken down in soil and in water. The half-life
in both of these environments is between 1 and 3 days. It does not readily
leach from soil, and it is not expected to be a groundwater pollutant.
Rotenone breaks down readily by exposure to sunlight. Nearly all of the
toxicity of the compound is lost in 5 to 6 days of spring sunlight or 2 to
3 days of summer sunlight.
Breakdown in vegetation: Rotenone is a highly active but
short-livedphotosensitizer. This means that an organism consuming the
compound develops a strong sensitivity to the sun for a short time. A
number of photodecomposition products are formed when bean leaves are
exposed to light. It is also sensitive to heat, with much of the rotenone
quickly lost at high temperatures.