Toxicity of Metals II | PHM 450 - Intro to Chemical Toxicology, Quizzes of Pharmacology

Class: PHM 450 - Intro to Chemical Toxicology; Subject: Pharmacology and Toxicology; University: Michigan State University; Term: Spring 2015;

Typology: Quizzes

2014/2015

Uploaded on 03/02/2015

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TERM 1
Absorption of As
DEFINITION 1
Inorganic arsenic is well absorbed (80-90%) from the GI tract.
TERM 2
Distribution of As
DEFINITION 2
Crosses placental barrier after high dose exposure
TERM 3
Biotransformation of As
DEFINITION 3
Reduction reactions of As5+ to As3+.As3+ is often
metabolized by methylation in the liver.
TERM 4
Excretion of As
DEFINITION 4
Via urine and feces.
TERM 5
Half Life of As
DEFINITION 5
10-30 hours.
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Absorption of As

Inorganic arsenic is well absorbed (80-90%) from the GI tract. TERM 2

Distribution of As

DEFINITION 2 Crosses placental barrier after high dose exposure TERM 3

Biotransformation of As

DEFINITION 3 Reduction reactions of As5+ to As3+.As3+ is often metabolized by methylation in the liver. TERM 4

Excretion of As

DEFINITION 4 Via urine and feces. TERM 5

Half Life of As

DEFINITION 5 10-30 hours.

Absorption of Hg

Liquid mercury is poorly absorbed from GI tract and skin.Vapor is readily absorbed from the respiratory tract. Methylated forms are highly lipophilic and therefore, readily absorbed. TERM 7

Distribution of Hg

DEFINITION 7 Hg0 and CH3Hg but not Hg2+ can cross blood-brain and placental barrier. TERM 8

Biotransformation of Hg

DEFINITION 8 Hg0 is oxidized to Hg2+, which is more readily absorbed. TERM 9

Excretion of Hg

DEFINITION 9 Via urine and feces. TERM 10

Half Life of Hg

DEFINITION 10 Hg0 and Hg2+ = 40 days.CH3Hg = 70 days.

Absorption of Cd

Cd is very poorly absorbed through the GI tract (5- 8%).Enhanced by dietary deficiencies in Ca and Fe. TERM 17

Distribution of Cd

DEFINITION 17 About 50-70% of the retained Cd is found in the liver and kidney.Cd can not cross the placental barrier. TERM 18

Biotransformation of Cd

DEFINITION 18 Cd binds to the albumin and metallothionein (MT). TERM 19

Excretion of Cd

DEFINITION 19 Poorly excreted through urine and feces. TERM 20

Half Life of Cd

DEFINITION 20 6-38 years in human kidney.4-19 years in human liver.

Absorption of Ni

Soluble compounds are the most rapidly and completely absorbed from the respiratory and/or GI tract.Less soluble nickel compounds are absorbed through the skin. TERM 22

Distribution of Ni

DEFINITION 22 Ni is transported by binding to albumin and nickel plasmin.Ni can cross placental barrier. TERM 23

Excretion of Ni

DEFINITION 23 Via urine and feces. TERM 24

Half Life of Ni

DEFINITION 24 7-39 hours in human plasma and urine. TERM 25

Absorption of Cr

DEFINITION 25 Cr6+ is absorbed much quicker than Cr3+.

Mechanism of As3+ Tox

Binds to sulfhydryl groups (-SH), thus reacts to a variety of proteins and inhibits their activity.Pyruvate dehydrogenaseGlutathione reductaseThioredoxin reductase TERM 32

Mechanism of As5+ Tox

DEFINITION 32 As5+ can kill cells by interfering with mitochondrial function.Mitochondria possess the electron transport chain and ultimately form ATP.Arsenate mimics phosphate. TERM 33

Hg

Toxicity

DEFINITION 33 Target organs: CNS (vapor, organic forms), kidney (mercuric salts), GI tract (mercuric salts).Biological effects: Neurotoxicity (sensory deficits, motor deficits - ataxia, mental retardation), ulceration and necrosis of GI tract, renal failure, and death. TERM 34

Mechanism of Hg Tox

DEFINITION 34 Hg alters protein phosphorylation.Hg has a particular affinity of proteins with sulfhydryl groups (-SH), which effects enzymes involved in the protein repair and oxidative damage prevention.CNS is critical target of Hg because cells that have the least ability to repair are the most sensitive. TERM 35

Pb

Toxicity

DEFINITION 35 Multiple target organs: CNS, kidney, and red blood cells.Carcinogenic: Lung and digestive system cancers.Biological effect: Could be acute or chronic.Acute: encephalopathy, lethargy, ataxia, coma, death.Chronic: developmental problems, lower IQ, decreased speech and language.

Pb - Mechanisms of CNS Tox

Pb serves as surrogate for Ca in the CNS. Pb blocks Ca entry into cells. Pb promotes neurotransmitter release in resting state but blocks NT release when an action potential is taking place. Pb inhibits mitochondrial uptake of Ca, thereby decreasing energy. Pb inhibits phospholipase C which is involved in long term memory. Pb interferes with Ca-dependent proteins, such as Calmodulin. TERM 37

Pb - Mechanisms of Hematotoxicity

DEFINITION 37 Pb serves as a surrogate for Fe in red blood cells. Pb shortens the life span of red blood cells. Pb impairs heme synthesis resulting in development of anemia. Inhibits delta-aminolevulinic acid dehydratase (ALAD). Inhibits ferrochelatase. TERM 38

Cd

Toxicity

DEFINITION 38 Multiple target organs: Lung, kidney, skeletal, CV system.Carcinogenic: Lung cancer.Biological effects: Abdominal pain, nausea, vomiting, COPD, renal failure, and cancer. TERM 39

Cd - Mechanisms of Renal Tox

DEFINITION 39 Cd accumulates in the kidney and liver after binding to metallothionine (MT).Cd is toxic to cells of the kidney (likely due to the release of Cd from MT) which then promotes inflammation. TERM 40

Ni

Toxicity

DEFINITION 40 Target organs: Lungs and skin.Carcinogenic: Lung cancers.Biological effects: Dermatitis, GI problems, headache, respiratory failure, cancer, and death.