The castor bean plant of castor plant is found in warm tropical regions. The main toxic substance of the castor plant is ricin. Ricin is one of the most poisonous substances known to us.
The map above shows the distribution of castor plants worldwide.
Effects and Action of Ricin
Toxicokinetics
Ricin is a large protein molecule which is poorly absorbed from the gastrointestinal tract. Ricin is better absorbed through the lungs and shows its toxic effects more through this route.
Toxicity and Symptoms
Abdominal pain, burning throat pain, nausea, vomiting, bloody diarrhea leading to dehydration, hypotension, seizure and multi organ failure.
Target organs
Ricin appears to be readily absorbed by inhalation, but dermal absorption is unlikely to occur through intact skin. Intravenously administered ricin distributes primarily to spleen, kidneys, heart, and liver, and intramuscularly administered ricin distributes to draining lymph nodes.
Historical or unique exposures
There have been many historical attempts to mail letters with ricin to poison people especially those in positions of power.
Treatments
Treatments are with activated charcoal, electrolyte replacement, and IV fluids.
Benzene is formed from both natural processes and human activities. Natural sources of benzene include volcanoes and forest fires. Benzene is also a natural part of crude oil, gasoline, and cigarette smoke.
Biotransformation
The above diagram shows how Benzene is transformed in the body.
Toxicokinetics
Carcinogenicity
Benzene is a known human carcinogen by regulatory agencies around the world. The IARC classifies benzene as a Group 1 carcinogen.
Mechanism of Action
Mechanism of action of benzene in hematotoxicity. Benzene suppresses the cell cycle by p53-mediated overexpression of p21, a cyclin-dependent kinase inhibitor, resulting not simply in suppression of hemopoiesis but rather in a dynamic change of hemopoiesis during and after benzene exposure.
Target organ
Bone marrow is the target organ for benzene and the liver is the main organ of metabolism for benzene.
Signs and symptoms of toxicity
Adverse effect of benzene is hematopoietic toxicity, which precedes leukemia. Chronic, high benzene exposure can lead to bone marrow damage, which may be manifest initially as anemia, leukopenia, thrombocytopenia, or a combination of these.
Genetic susceptibility or heritable traits
A study in mice either expressing the gene for NAD(P)H: quinone oxidoreductase-1 (NQO1) or lacking the gene found a 9 fold increase in micronucleated reticulocytes compared with a 3-fold increase in mice with the gene.
Historical or unique exposures
Because of benzene’s volatility and solvent properties, it was used in the printing industry in inks, ink solvents, and cleaning agents from the 1930s to the 1970s. Typical benzene air concentrations, considering both personal and area samples of various durations, were as high as 200 p.p.m. in the 1930s through the 1950s, 3-35 p.p.m. in the 1960s, 1.3-16 p.p.m. in the 1970s, 0.013-1 in the 1980s, and far less than 1 p.p.m. in the 1990s and 2000s.
Treatments
Benzene poisoning needs to be treated with medial care. There is not antidote for benzene poisoning and the best that can be done is to seek medical attention.
Biomarkers
Benzene in alveolar air, unmetabolized benzene, and ttMA in urine are potential biomarkers for occupational benzene exposure. The main marker here is the ttMA in urine. It is interesting to see that benzene itself is used to determine if exposure if significant.
Bruckner J.V., & Anand S, & Warren D (2013). Toxic effects of solvents and vapors. Klaassen C.D.(Ed.),Casarett and Doull’s Toxicology: The Basic Science of Poisons, Eighth Edition. McGraw-Hill. https://accesspharmacy-mhmedical-com.proxy.lib.ohio-state.edu/content.aspx?bookid=958§ionid=53483749
Yoon BI, Hirabayashi Y, Kawasaki Y, et al. Mechanism of action of benzene toxicity: cell cycle suppression in hemopoietic progenitor cells (CFU-GM). Exp Hematol. 2001;29(3):278-285. doi:10.1016/s0301-472x(00)00671-8
We get most of the molybdenum we need through our diet. We do not need a lot of it in our diet. We only need about 45ug a day for bodily functions. Molybdenum was first separated from graphite and lead in 1778. It is described as lead like and its name comes from a Greek word meaning lead like.
Benefits of Molybdenum
Molybdenum is a trace mineral but, very important in the roles it plays in the body.
Molybdenum Deficiency
Molybdenum cofactor (Moco) deficiency is a pleiotropic genetic disorder characterized by the loss of the molybdenum-dependent enzymes sulfite oxidase, xanthine oxidoreductase, and aldehyde oxidase, due to mutations in the genes involved with Moco biosynthesis.
Other than hearing about molybdenum probably sometime in chemistry it is not something often discussed. It is essential for life and is important in synthesis of four specific co-factors.
Toxicity
Molybdenum is not very toxic to humans. In rare cases of high exposure or consumption side effects of high uric acid levels in serum and urine and a gout like syndrome have been observed. Human research is limited and most of what is know about molybdenum is from animal testing. When inhaled metallic and soluble molybdenum trioxide have been reported to cause pneumoconiosis. Recent animal models have shown that exposure to copper and molybdenum can effect male reproductive health. In many ways molybdenum toxicity is like copper deficiency.
Treatments
For someone that is exposed to very high levels of Molybdenum copper can be used to reverse the effects. Molybdenum is used in the treatment of patients with Wilson’s disease. Treatment with molybdenum may also be beneficial for angiogenesis, inflammation, and other disorders associated with excess copper.
Molybdenum Mechanism of action
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Here you can see the enzymes and co-factors that molybdenum is used in and how it works in the body.
Toxicokinetics
Water-soluble molybdenum is readily absorbed when ingested. In animals 75% and 95% is absorbed while in humans it ranges from 28% to 77%. Once absorbed molybdenum is rapidly present in the blood and the highest concentrations are present in the kidneys, liver, and bones. When elevated exposure is stopped levels quickly return to normal. The metabolism of molybdenum is similar to copper and sulfur. Exposure to molybdenum decreases copper and sulfate uptake. Most of the molybdenum is excreted in the urine and less than a percent is excreted in the bile. Depending on diet the uptake and retention of molybdenum can very to what the body needs.
Conclusion
Molybdenum is a fairly safe metal that our bodies need. We get enough from our daily diets and do not need to worry to much about deficiencies. The carcinogenicity of molybdenum is low but as with anything to much can be toxic and lead to problems.
References:
ar E.J., & Boyd W.A., & Freedman J.H., & Waalkes M.P. (2013). Toxic effects of metals. Klaassen C.D.(Ed.),Casarett and Doull’s Toxicology: The Basic Science of Poisons, Eighth Edition. McGraw-Hill. https://accesspharmacy-mhmedical-com.proxy.lib.ohio-state.edu/content.aspx?bookid=958§ionid=53483748
1,3 dichloropropene is a organochlorine compound that is a colorless liquid and smells sweet. It dissolves in water and evaporates easily. It is used as a pesticide, typically as preplant fumigant and nematicide. Exposure to 1,3-dichloropropene, may occure dermally or by inhalation, during its manufacture, formulation, or application as a soil fumigant. The public may be exposed by inhalation near an area using it as a fumigant or from consumption of contaminated water near hazardous waste sites.
The above diagram shows the absorption and mechanism of action in the body of 1,3 dichloropropene.
1,3 dichorpropene toxicokinetics in humans appears to be similar to those observed in rodents. Inhalation studies in humans and rodents have shown the vapors to be readily absorbed, conjugated with glutathione (GSH) thru glutathione S-transferase (GST). 1,3 dichloropropene is rapidly excreted in the urine as N-acetyl-(S-3-chloroprop-2-enyl)cysteine (3CNAC), a mercapturic acid metabolite. 1,3 dichloropropene is unlikely to accumulate in the body.
The above diagram shows the bio transformation of 1,3 dichloropropene.
Carcinogenicity of 1,3 dichoropropene in humans is limited. There have been only two reported cases of histiocytic lymphomas and one case of leukemia have been reported in emergency response personnel. 1,3-dichloropropene is classified as a Group B2 probable human carcinogen. Forestomach and liver tumors were observed in rats via gavage and also occurred when exposed to 1,3 dichloropropene in the diet.
The target organs of 1,3 dichloropropene are eyes, skin, respiratory system, central nervous system, liver, and kidneys.
Symptoms of toxicity are irritation eyes, skin, respiratory system; eye, skin burns; lacrimation, headache, dizziness; in animals; liver, and kidney damage.
Biomarkers for damage and exposure to 1,3 dichlopropene are no different from renal or serum and there are no markers for long term exposure.
A study in male mice showed an increase incidence of bronchioalveolar adenomas through inhalation. This same thing does not occur in female mice or rats.
Treatment does not exist for acute or chronic exposure to 1,3 dichloropropene.
