Mercury Toxicity: Sources, Mechanism, and Treatment

 
Heavy Metal Toxicity
Heavy Metal Toxicity
(
(
Mercury
Mercury
)
)
 
 
Presented by:-
                                            Dr.Archana
                    Assistant Professor_cum_Jr .Scientist
                     Deptt.Of Pharmacology & Toxicology
                              Bihar Veterinary College, Patna
 
Content of chapter
Content of chapter
 
   
  * Sources
    * Toxicokinetic
    * Mechanism of toxicity
    * Clinical Signs
    *  Treatment
 
Sources
Sources
 
 Mercury poisoning is a common occurrence in
both human and animal populations. Mercury
exists naturally in the environment, and as a result
everyone is exposed to very low levels. Aristotle
named it 
“Quicksilver”
.
 
  Mercury exists in a variety of chemical forms,
including ---
  
Elemental mercury
 (Thermometers, light bulbs),
  
Inorganic mercurial
 (Mercuric or Mercurous)
  
Organic mercury
 (Methyl, or Ethyl).
 
Continue...
Continue...
 
 * Methylmercury is of particular concern
because it can bioaccumulate in certain
edible freshwater and saltwater fish As a
result, the larger and older fish living in
contaminated water build up levels of
mercury in their bodies.
 
*  The release of methylmercury into an ocean
bay (Minamata) in Japan in the 1950s led to a
massive health disaster, and the clinical
syndrome was named 
Minamata disease
.
Thousands of people were poisoned,and
hundreds of them had severe brain damage.
 
Continue...
Continue...
 
 * Methylmercury is of particular concern
because it can bioaccumulate in certain
edible freshwater and saltwater fish As a
result, the larger and older fish living in
contaminated water build up levels of
mercury in their bodies.
 
*  The release of methylmercury into an ocean
bay (Minamata) in Japan in the 1950s led to a
massive health disaster, and the clinical
syndrome was named 
Minamata disease
.
Thousands of people were poisoned,and
hundreds of them had severe brain damage.
 
Toxicokinetics :-
Toxicokinetics :-
 
Elemental mercury( mercury vapour):-
 
   It is not particularly toxic when   ingested orally
snide it is not absorbed through GIT.
 
 Accidental spilling of metal in poorly ventilated room
often in scientific lab can produce toxic effect in
man.
 
  The vapour of mercury can cross the cell membrane
and is absorb through lung.
 
  CNS toxicity is more prevalent after exposure to
mercury vapour than to the ingestion of mercury
salt.
 
Continue…
Continue…
 
Inorganic mercury :-
 
 
Absorption is poor to the extent of 2- 10%.
 
  It is distributed non-uniformly after absorption; highest
concentration of mercury is found in kidney where it is
retained for a long period.
 
  Concentartion of mercury are similar in whole blood and
placenta.
 
  Inorganic mercury do not crosses  blood brain barrier.
 
t is excreted via urine and stool.
 
Continue…
Continue…
 
Organic Mercury :-
 
 
 It is more completely absorbed from the GIT
then inorganic form. Intestinal absorption of
organic mercury  may be as high as 95% of the
dose given.
 
  It crosses the placental barrier and blood
brain barrier hence produce more neurological &
teratogenic effect than inorganic form.
 
 Major route of excretion is through faeces;
they are also readily excreted via urine.
 
Mechanism of  Toxicity
Mechanism of  Toxicity
 
Inorganic mercury
   
The biochemical basis of the mechanism of toxicity of
mercury is due to its interaction with dithiol group of protein
and precipitate it, i.e it interferes with protein metabolism
and their corrosive action directly damage the GIT mucosa.
  It is recorded that about 50 enzymes are inhibited by low
concentration of mercuric ion.
 
organic mercury
The mechanism of toxicity is similar to that of
inorganic mercurial but the toxicity is greater than
inorganic mercurial because being high lipid soluble
they are
  * easily absorp through GIT
  *crosses different cellular membrane
  * 
crosses PB & BBB hence causes harmful teratogenic
& neurotoxic effects
 
 
Clinical signs
Clinical signs
 
Inorganic mercury:-
Acute – mainly the effect GIT & Kidney
 
GIT –
 
The symptoms are
 
 metallic taste in
mouth, abdominal pain, diarrhoea with
blood in the faeces leading to
dehydration.
  
Kidney –
 
Oligoura followed by anuria,
albuminuria, and uraemia.
 
 Chronic –
 
kidney damage is the main
symptom. Increase urinary excretion of
alkaline phosphatase is found to be
sensitive indicator of kidney damage.
 
Continue....
Continue....
 
 In man cumulative poisoning due to
continued absorption of small
amount over a long period leads to
profuse salivation, swelling of gums,
loosening of gum and teeth and
necrosis of jaw bones. These
symptoms constitute what is known
as  
mercurial ptyalism
 
 
 
 
organic mercury
organic mercury
 
 
The main symptoms are those of
nervous disturbances; namely nerve
pain, blindness, excitation, abnormal
behaviour & chewing, incordination
and convulsion. Neurological signs
may be irreversible once they
develop.
 
Treatment
Treatment
 
  
Specific treatment:-
  
BAL (British anti-lewisite )  @ 3 mg/kg, IM, every 4 hr
for the first 2 days, every 6 hr for the third day, and 12
hrly  for the next 10 days or until recovery.
 
D-Penicillamine is used as an antidote in the human being.
 
Non-specific treatment:-
  * 
Gastric lavage for removal of poison from the GIT.
   * Administration of proteinous liquid to protect the GIT.
 
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Mercury toxicity, a common occurrence in humans and animals, poses serious health risks. This includes exposure from elemental, inorganic, and organic forms of mercury. Methylmercury bioaccumulation in fish can lead to severe health consequences, as seen in past incidents like Minamata disease. Understanding the toxicokinetics of different mercury forms is crucial for effective prevention and treatment strategies.

  • Mercury Toxicity
  • Heavy Metal Poisoning
  • Methylmercury
  • Toxicokinetics
  • Treatment

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  1. Heavy Metal Toxicity (Mercury) Presented by:- Dr.Archana Assistant Professor_cum_Jr .Scientist Deptt.Of Pharmacology & Toxicology Bihar Veterinary College, Patna

  2. Content of chapter * Sources * Toxicokinetic * Mechanism of toxicity * Clinical Signs * Treatment

  3. Sources Mercury poisoning is a common occurrence in both human and animal populations. Mercury exists naturally in the environment, and as a result everyone is exposed to very low levels. Aristotle named it Quicksilver . Mercury exists in a variety of chemical forms, including --- Elemental mercury (Thermometers, light bulbs), Inorganic mercurial (Mercuric or Mercurous) Organic mercury (Methyl, or Ethyl).

  4. Continue... * Methylmercury is of particular concern because it can bioaccumulate in certain edible freshwater and saltwater fish As a result, the larger and older fish living in contaminated water build up levels of mercury in their bodies. * The release of methylmercury into an ocean bay (Minamata) in Japan in the 1950s led to a massive health disaster, and the clinical syndrome was named Minamata disease. Thousands of people were poisoned,and hundreds of them had severe brain damage.

  5. Continue... * Methylmercury is of particular concern because it can bioaccumulate in certain edible freshwater and saltwater fish As a result, the larger and older fish living in contaminated water build up levels of mercury in their bodies. * The release of methylmercury into an ocean bay (Minamata) in Japan in the 1950s led to a massive health disaster, and the clinical syndrome was named Minamata disease. Thousands of people were poisoned,and hundreds of them had severe brain damage.

  6. Toxicokinetics :- Elemental mercury( mercury vapour):- It is not particularly toxic when ingested orally snide it is not absorbed through GIT. Accidental spilling of metal in poorly ventilated room often in scientific lab can produce toxic effect in man. The vapour of mercury can cross the cell membrane and is absorb through lung. CNS toxicity is more prevalent after exposure to mercury vapour than to the ingestion of mercury salt.

  7. Continue Inorganic mercury :- Absorption is poor to the extent of 2- 10%. It is distributed non-uniformly after absorption; highest concentration of mercury is found in kidney where it is retained for a long period. Concentartion of mercury are similar in whole blood and placenta. Inorganic mercury do not crosses blood brain barrier. t is excreted via urine and stool.

  8. Continue Organic Mercury :- It is more completely absorbed from the GIT then inorganic form. Intestinal absorption of organic mercury may be as high as 95% of the dose given. It crosses the placental barrier and blood brain barrier hence produce more neurological & teratogenic effect than inorganic form. Major route of excretion is through faeces; they are also readily excreted via urine.

  9. Mechanism of Toxicity Inorganic mercury The biochemical basis of the mechanism of toxicity of mercury is due to its interaction with dithiol group of protein and precipitate it, i.e it interferes with protein metabolism and their corrosive action directly damage the GIT mucosa. It is recorded that about 50 enzymes are inhibited by low concentration of mercuric ion. organic mercury The mechanism of toxicity is similar to that of inorganic mercurial but the toxicity is greater than inorganic mercurial because being high lipid soluble they are * easily absorp through GIT *crosses different cellular membrane * crosses PB & BBB hence causes harmful teratogenic & neurotoxic effects

  10. Clinical signs Inorganic mercury:- Acute mainly the effect GIT & Kidney GIT The symptoms are metallic taste in mouth, abdominal pain, diarrhoea with blood in the faeces leading to dehydration. Kidney Oligoura followed by anuria, albuminuria, and uraemia. Chronic kidney damage is the main symptom. Increase urinary excretion of alkaline phosphatase is found to be sensitive indicator of kidney damage.

  11. Continue.... In man cumulative poisoning due to continued absorption of small amount over a long period leads to profuse salivation, swelling of gums, loosening of gum and teeth and necrosis of jaw bones. These symptoms constitute what is known as mercurial ptyalism

  12. organic mercury The main symptoms are those of nervous disturbances; namely nerve pain, blindness, excitation, abnormal behaviour & chewing, incordination and convulsion. Neurological signs may be irreversible once they develop.

  13. Treatment Specific treatment:- BAL (British anti-lewisite ) @ 3 mg/kg, IM, every 4 hr for the first 2 days, every 6 hr for the third day, and 12 hrly for the next 10 days or until recovery. D-Penicillamine is used as an antidote in the human being. Non-specific treatment:- * Gastric lavage for removal of poison from the GIT. * Administration of proteinous liquid to protect the GIT.

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