Eine sehr empfehlenswerte Internetseite, die für alle gängigen Substanzen Toxikologische Profile anbietet:

Der Index findet sich hier:

http://www.atsdr.cdc.gov/

Wie finde ich z.B. das Profil von Acetone?

>Im Index auf A

>Acetone anklicken

>Toxicological Profile anklicken (findet sich etwa in der Seitenmitte)

>Download von PDF Version, 4.3 MB = 276 Seiten

Blei wird z.B. auf 625 Seiten beschrieben. (Download von PDF Version, 6.2 MB)

http://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=96&tid=22

MfG

[ironie] Na dann! Einmal durch den Google-Übersetzer und wir haben unsere Datenbank [/ironie]

Aber netter Link, Danke!

@ NI2: English my dear, wie Huxley
@ Chemdoc: Danke für den Link

Der Link ist Klasse. Aber alles haben die auch nicht. Tellur habe ich z.B. nicht gefunden und Selen wird auch sehr knapp abgehandelt. Trotzdem eine wirklich gute und zitierfähige Quelle.

Selen ist allgemein ein wenig schwierig,...

Um es mit Loriot zu sagen: "Ach was..."
Ich habe bisher nur rausgefunden, dass es Disulfidbrücken mag und ähnlich wie Tellur wirkt. Muss doch mehr, in knapper Form dazu
geben...

Ist richtig,... die meisten Bücher die ich gerade hier habe handeln das ganze auch nur recht kurz ab. Ich kram mal eben die Physiologische Chemie raus

Mach dir keinen Stress. Hau mich jetzt afs Ohr. In viereinhalb Stunden ist die Nacht für mich vorbei...

Brachte eh nicht viel -.- nur ein bissel Info zur Glutathionperoxidase...

Im Daunderer finde ich bisher auch noch nix, werde - wenn ich dran denke - nochmal nach komplett neuer Literatur schauen.

UPDATE: 550 Seiten nur über Selen gefunden

Mal eine kurze Ausführung zur Toxikologie von Selen:
Das Sheet erklärt alles hier genannte auf den nächsten paar hundert Seiten wesentlich ausführlicher.

"[...]

HOW CAN SELENIUM ENTER AND LEAVE MY BODY?

Selenium from the environment mainly enters the body when people eat food containing selenium.
The human body easily absorbs the organic selenium compounds (for example,
selenoamino acids) when eaten and makes them available where needed in the body.
The selenium in drinking water is usually in the form of inorganic sodium selenate and sodium
selenite; these are also easily absorbed from the digestive tract. The human body can
change these inorganic selenium compounds into forms it can use. Selenium in the air
may also enter your body when you breathe it.
Most of the selenium that enters the body quickly leaves the body, usually within 24 hours.
Beyond what the body needs, selenium leaves mainly in the urine, but also in feces and breath.
Selenium can build up in the human body, however, if exposure levels are very high or if exposure
occurs over a long time. It builds up mostly in the liver and kidneys but also in the blood, lungs,
heart, and testes. Selenium can build up in the nails and in hair, depending on time and amount of
exposure.

HOW CAN SELENIUM AFFECT MY HEALTH?

The general public rarely breathes high levels of selenium, although some people may be
exposed to selenium dust and selenium compounds in workplace air. Dizziness, fatigue, and
irritation of mucous membranes have been reported in people exposed to selenium in workplace
air at concentrations higher than legal levels. In extreme cases, collection of fluid in the lungs
(pulmonary edema) and severe bronchitis have been reported.
The normal intake of selenium by eating food is enough to meet the RDA of 55 μg/day for adults
for this essential nutrient.
Intentional or accidental swallowing of a large amount of sodium selenate or sodium selenite (for
example, a very large quantity of selenium supplement pills) could be life-threatening without
immediate medical treatment. Even if mildly excessive amounts of selenium are eaten over long
periods, brittle hair and deformed nails can develop. In extreme cases, people may lose feeling
and control in arms and legs. These health effects, called selenosis, were seen in several villages
in China where people were exposed to foods high in selenium for months to years.
Upon contact with human skin, selenium compounds have been reported to cause rashes,
redness, heat, swelling, and pain. Brief, acute exposure of the eyes to selenium dioxide as a dust
or fume in workplace air may result in burning, irritation, and tearing. However, only people
who work in industries that process or use selenium or selenium compounds are likely to come
into contact with levels high enough to cause eye irritation.
Studies of laboratory animals and people show that most selenium compounds probably do not
cause cancer. In fact, studies of cancer in humans suggest that lower-than-normal selenium
levels in the diet might increase the risk of cancer. But levels of selenium in the diet that are
much higher than normal have not been shown to reduce the risk of cancer in humans. Taking
selenium so that your daily amount is greater than that required may just increase your risk of
selenium poisoning.
Based on studies up until 1987, the International Agency for Research on Cancer (IARC)
determined that selenium and selenium compounds could not be classified as to their ability to
cause cancer in humans. However, since then the EPA has determined that one specific form of
selenium, called selenium sulfide, is a probable human carcinogen. Selenium sulfide is the only
selenium compound shown to cause cancer in animals. Rats and mice that were fed selenium
sulfide daily at very high levels developed cancer. Selenium sulfide is not present in foods, and
it is a very different chemical from the organic and inorganic selenium compounds found in
foods and in the environment.
Very high amounts of selenium have resulted in decreased sperm counts, increased abnormal
sperm, changes in the female reproductive cycle in rats, and changes in the menstrual cycle in
monkeys. The relevance of the reproductive effects of selenium exposure in animals studied to
potential reproductive effects in humans is not known. Selenium compounds have not been
shown to cause birth defects in humans or in other mammals.


HOW CAN SELENIUM AFFECT CHILDREN?
This section discusses potential health effects from exposures during the period from
conception to maturity at 18 years of age in humans.

Children living near selenium waste sites or coal burning plants are likely to be exposed to higher
environmental levels of selenium through breathing, touching soil, and eating contaminated soil.
Children living in areas of China with high selenium in the soil had higher levels of selenium in
the blood than adults from that area. Very few studies have looked at how selenium can affect
the health of children. Children need small amounts of selenium for normal growth and
development. Children will probably show the same sort of health effects from selenium
exposure as adults, but they may be less susceptible to health effects of selenium than adults.
We do not know if exposure to selenium will result in birth defects in people. Selenium
compounds have not been shown to cause birth defects in humans or in other mammals. We
have no information to suggest that there are any differences between children and adults in
where selenium is found in the body or in how fast it enters or leaves the body. Studies in
laboratory animals have shown that selenium crosses the placenta and enters the fetus. Studies in
humans show that infants are supplied with selenium through breast milk, and therefore, women
who were exposed to selenium by living near a waste site might transfer selenium to their babies.
However, babies in areas of China with high selenium in the soil did not show any signs of health
effects due to selenium, even though some of their parents did.

SUMMARY OF HEALTH EFFECTS

Selenium is known to be an essential micronutrient for humans and other animals; both inadequate and
excessive selenium intake can cause adverse health effects. However, most people in the United States
are unlikely to suffer from selenium deficiency. The current recommended dietary allowance (RDA) for
selenium established by the Food and Nutrition Board of the National Research Council is 55 μg/day for
adults. Adverse health effects due to selenium are generally observed at doses at least 5 times greater
than the RDA.
Selenium deficiency has been associated with two endemic diseases found in selenium-poor regions of
China: a cardiovascular condition known as Keshan Disease and an osteoarthropathy called Kashin-Beck
Disease. Keshan Disease is characterized by cardiac enlargement, abnormal ECG patterns, cardiogenic
shock, and congestive heart failure, with multifocal necrosis of the myocardium. The disease is reported
to occur primarily in children and women of child-bearing age and has been successfully treated by
selenium supplementation; however, a low incidence of cases persisting after selenium supplementation
suggests that there may be other contributing factors. Kashin-Beck Disease is characterized by atrophy,
degeneration, and necrosis of cartilage tissue, and occurs primarily in children between the ages of 5 and
13 years; it also has been successfully treated with selenium supplements. Chronically ill people and
older people have been shown to have lower organ concentrations of selenium than healthy individuals,
but it is not clear if this is a cause or consequence of aging or illness.
The primary target organ in humans and laboratory animals in cases of acute, high-level inhalation
exposure to selenium is the lung, with cardiovascular, hepatic, nervous, and renal involvement as well.
Lesser effects are observed in other organs/organ systems. Workers exposed to high concentrations of
elemental selenium dust reported stomach pain and headaches, while workers briefly exposed to high
levels of selenium dioxide dust reported respiratory symptoms such as pulmonary edema, bronchial
spasms, symptoms of asphyxiation and persistent bronchitis, elevated pulse rates, lowered blood
pressure, vomiting, nausea, and irritability. No studies were located regarding effects in humans or
animals after intermediate-duration inhalation exposure to selenium or to selenium compounds. For
chronic inhalation exposure, there are several occupational studies that describe respiratory effects such
as irritation of the nose, respiratory tract, and lungs, bronchial spasms, and coughing following exposure
to selenium dioxide or elemental selenium dust. Respiratory symptoms similar to those reported for
humans have been seen in animals inhaling high doses of elemental selenium fumes or dust, and studies
of animals with acute inhalation exposure to hydrogen selenide or elemental selenium fumes or dust have
reported hepatocellular degeneration and atrophy of the liver.
Acute oral exposure to high concentrations of selenium produces nausea, vomiting, and diarrhea in both
humans and animals. Acute exposure of humans to selenium has occasionally produced cardiovascular
symptoms, such as tachycardia, but no electrocardiographic abnormalities were found in 20 individuals
from a human population chronically exposed to selenium. In contrast, acute and intermediate oral
exposure of laboratory animals to selenium has produced myocardial degeneration.
Chronic oral exposure to high concentrations of selenium compounds produces selenosis, the major
effects of which are dermal and neurological. As evidenced by populations in China, chronic exposure to
high selenium levels in the diet can cause diseased nails and skin and hair loss. Higher levels can cause
neurological problems including unsteady gait and paralysis. In contrast, however, studies of
contemporary human populations living in areas of naturally occurring high selenium concentrations in
the United States have not revealed adverse health effects in those populations. This difference may
result from the lower exposure observed in the U.S. population compared to the Chinese population, as
well as a better balanced, higher protein diet in the United States, which may increase tolerance to
selenium.
Intermediate and chronic oral exposure of livestock to high levels of dietary selenium compounds also
produces dermal and neurological effects. Studies in animals with high selenium concentrations
demonstrate that many organ systems retain selenium and are affected. The primary effects in laboratory
animals exposed to inorganic selenium salts or to selenium-containing amino acids are cardiovascular,
gastrointestinal, hematological, hepatic, dermal, immunological, neurological, and reproductive. Blind
staggers has been repeatedly observed in cattle feeding off vegetation in areas with high selenium content
in the soil. However, the neurological effects have not been replicated in experimentally-exposed cattle
receiving doses of selenium sufficient to induce hoof lesions, and thus, the neurological symptoms
associated with blind staggers may be due to other compounds found within this vegetation.
Some evidence for adverse effects on the endocrine system has also been found following intermediate
and chronic oral exposure to elevated levels of dietary selenium in humans and animals. Human studies
have demonstrated a decrease in triiodothyronine levels in response to increased dietary selenium,
although the hormone levels remained within the normal range. Intermediate-duration studies of rats
have shown reductions in type-I-deiodinase activity in response to selenium. However, the levels of
thyroid hormones in these animals did not show a consistent pattern.
There is no evidence to support a causal association between selenium compounds and cancer in humans.
In fact, some epidemiological and experimental evidence suggests that selenium exposure under certain
conditions may contribute to a reduction in cancer risk. Currently, the chemopreventive potential of
selenium is under research. Selenium sulfide and ethyl selenac are the only selenium compounds that
have been shown to be carcinogenic upon oral administration in rodents; however, significant exposure
to these forms of selenium is extremely unlikely.
Studies of Chinese populations and laboratory animals exposed to high levels of organic and/or inorganic
selenium compounds have not found evidence of selective teratogenic effects in mammals.

Selenosis.
Following chronic oral exposure to excessive amounts of the organic selenium
compounds found in food, the two principal clinical conditions observed in humans are dermal and
neurological effects, as described most completely in the epidemiological study of endemic selenosis in
the People's Republic of China. The dermal manifestations of selenosis include loss of hair, deformation
and loss of nails, and discoloration and excessive decay of teeth, while neurological effects include
numbness, paralysis, and occasional hemiplegia.
Similar clinical manifestations occur in livestock following intermediate and chronic exposure to
excessive amounts (more than 30 times the normal dietary amount of selenium) of the organic selenium
compounds found in seleniferous plants, including loss of hair and malformation of hooves in pigs,
horses, and cattle and poliomyelomalacia in pigs. Histologically, swine with selenium-induced
neurological signs exhibit bilateral macroscopic lesions of the ventral horn of the spinal cord. The
selenium in the selenium-accumulating plant Astragalus bisulcatus appears to be a more potent
neurotoxicant than D,L-selenomethionine or selenate. Following a similar dose of selenium, A. bisulcatus
resulted in complete paralysis in four of five pigs after 5 days of treatment, and in the last pig after
3 weeks of treatment, while in pigs fed selenate, three of five developed complete paralysis, and one pig
developed posterior paralysis after 4–21 days of treatment. Although D,L-selenomethionine resulted in
the greatest incidence of selenosis, it was the least potent neurotoxin, resulting in posterior paralysis in
two of five pigs after 9 and 24 days of treatment. The pigs that did not develop paralysis were fed
D,L-selenomethionine for approximately 31 days. The form of selenium in A. bisulcatus is unknown,
although Panter et al. indicate that it is nonprotein.
The neurological signs and histopathology observed in livestock following oral exposure to excess
selenium compounds have not been recorded in laboratory animals. This suggests that (1) small
laboratory mammals may not be appropriate models for selenium toxicity in humans (e.g., laboratory
animals absorb selenium compounds to a lesser extent, or metabolize and/or excrete selenium compounds
more quickly), (2) some as yet unidentified organic form of selenium contributes to the neurological
manifestations of chronic selenosis in humans and in livestock, or (3) unrecognized confounding factors,
such as other plant toxins, have contributed to the neurological syndrome associated with chronic
selenosis in field studies of humans and livestock.

Endocrine Effects.
Selenium is a component of all three members of the deiodinase enzyme family,
the enzymes responsible for deiodination of the thyroid hormones, and has a physiological role in the
control of thyroid hormone levels. Significant decreases in triiodothyronine levels in response to
elevated selenium have been observed in humans. However, the triiodothyronine levels observed in
these studies were within the normal human range, so the biological impact of this change is unclear.
The effect of increased dietary selenium on other thyroid hormones is also unclear. Intermediateduration
studies in rats show a decrease in type-I-deiodinase activity in response to elevated selenium;
however, the levels of thyroid hormones in these animals did not show any consistent changes.
One of the most common effects observed following excess selenium intake in animals is a decrease in
growth. It is likely that the selenium-induced reduction in growth has an endocrine component. For
example, selenite treatment of young rats decreased somatomedin C levels, and growth hormone
secretion in response to the growth hormone releasing factor was also reduced in selenium-treated rats.
The primary endocrine target of selenium leading to decreased growth has yet to be elucidated.
Pancreatic toxicity has been observed following excess selenium exposure. Cytoplasmic flocculation
was observed in lambs treated with a single oral dose of selenite, and pancreatic damage, which was not
further described, was noted in rats following chronic oral treatment with selenate or selenite. Pancreatic
toxicity associated with excessive selenium exposure is likely related to the unique ability of that organ
to accumulate the element.

Hepatic Effects.
Liver effects have not been reported for humans exposed to excessive amounts of
selenium. No significant abnormalities were found in blood levels of liver enzymes of individuals living
in high selenium areas, or in a “supersonic B” morphological examination of the livers of 20 individuals
suffering from severe symptoms of selenosis. In experimental and other animals, however, the liver has
been shown to be affected following both inhalation and oral exposure to several different selenium
compounds. Hepatocellular degeneration was observed in guinea pigs following inhalation exposure to
elemental selenium dust and hydrogen selenide. Cirrhosis, hepatocellular degeneration, and changes in
liver enzyme levels in serum have been reported for rats, pigs, and mice orally exposed to selenite,
selenate, or organic selenium. The doses in these studies producing adverse effects were approximately
10 times the amount normally found in an adequate diet. The liver appears to be the primary target organ
for the oral toxicity of selenium in experimental animals following intermediate and chronic exposure,
whereas liver cirrhosis or dysfunction has not been a notable component of the clinical manifestations of
chronic selenosis in humans. Selenium sulfide administration has also produced frank hepatotoxicity in
rats, but not in mice.

Renal Effects.
No reports of renal effects in humans were located. In nonhuman animals, mild
kidney effects have been observed following oral exposure to selenium compounds. These effects
include hydropic degeneration in sheep exposed to selenite and nephropathy in monkeys exposed to
selenomethionine. Rats appear to be more sensitive than mice to the renal effects of selenium
compounds. A dose-related increase in renal papilla degeneration, described as mild to minimal, was
observed in rats treated with selenate or selenite in the drinking water, while the only kidney effect noted
in mice treated with sodium selenate or selenite in the drinking water was increased kidney weight.
Selenium sulfide administration to mice has, however, been shown to produce interstitial nephritis.

Body Weight Effects.
Two of the most common effects in experimental animals following
intermediate or chronic oral administration of excessive inorganic and organic compounds of selenium
are reduced growth rate of young animals and loss of weight in older animals. Selenium sulfide
administration has been associated with reduced body weight in female mice. As noted under endocrine
effects, it is quite possible that the decreased growth rate has an endocrine component.

Reproductive Effects.
In samples from more than 200 men, no correlation between seminal fluid
selenium and sperm count or mobility was detected. No significant increase in spontaneous abortions
was reported among women chronically exposed to drinking water containing excessive amounts of
selenium. Oral or injection treatment of rats with sodium selenate or selenite (at doses at least 8 times
greater than those normally supplied by an adequate diet) has been shown to increase the number of
abnormal sperm, produce testicular hypertrophy, or degeneration and atrophy in males, and to affect the
estrous cycle in females. The animals in these studies were not mated, so it is not clear if fertility was
affected. A small increase in the number of abnormal length estrous cycles was observed in mice
exposed to selenium. Disturbances in the menstrual cycle (anovulation, short luteal and follicular
phases) were also observed in monkeys treated orally with L-selenomethionine. Selenium deficiency has
also been reported to cause decreased sperm production and motility in rats. The relevance of these
reproductive effects of selenium in laboratory animals to potential reproductive effects in humans is not
known.

[...]

aus:

DRAFT TOXICOLOGICAL PROFILE FOR SELENIUM

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
Public Health Service
Agency for Toxic Substances and Disease Registry

Ebenfalls zu empfehlen:

Selenium in Food and Health - Conor Reilly ISBN-10: 0-387-33243-X

Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium ans Carotinoids - Food and Nutrition Board Institute of Medicine ISBN 0-309-06949-1 (case) -- ISBN 0-309-06935-1 (paper)