Toksisitas Logam..
Transcript of Toksisitas Logam..
TOKSISITAS LOGAM BERATPENDAHULUAN
Orang-orang sudah selalu tepapar dengan logam berat di dalam lingkungan
Cemaran logam pada makanan dan air bisa menyebabkan keracunan
Kandungan logam pada pestisida dan zat-zat terapetik merupakan sumber pemaparan yang membahayakan
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Logam berat menimbulkan efek toksik dengan cara bergabung dengan satu atau lebih gugus reaktif (ligan) yang penting untuk fungsi fisiologis normal
Logam berat, khususnya dalam seri transisi pada sistem periodik, dapat bereaksi di dalam tubuh dengan ligan yang mengandung gugus :oxygen (-OH, -COO -, -OPO3H , >C=O), sulfur (-SH, -S-S-), nitrogen (-NH2 and >NH)
Logam berat yang paling mendapat perhatian akan toksisitasnya adalah
lead (Pb) mercury (Hg)arsenic (As) cadmium (Cd)
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TOKSISITAS LOGAM BERAT
TIMBAL (Pb) Sumber utama pemaparan lingkungan dari logam
adalah tinta, cat bertimbal dan air minum bertimbal.
Kebanyakan toksisitas yang berat dari lingkungan berasal dari pemaparan industri.
Makanan dan minuman asam dapat melarutkan timbal bila dikemas atau disimpan dalam wadah yang tidak tersepuh sempurna, dan dapat menyebabkan keracunan timbal yang fatal bagi manusia.
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Keracunan Timbal
Keracunan akut timbal relatif jarang dan terjadinya karena memakan senyawa timbal larut asam atau menghirup uap timbal
Aksi lokal pada mulut menimbulkan astringensia, rasa haus, dan rasa logam.
Mual, nyeri lambung, dan muntah Tinja berwarna hitam karena PbS,
dan mungkin terjadi diare ataupun konstipasi
Gejala akut pada SSP : paresthesia, and kelemahan otot
Krisis hemolytic akut : anemia berat and hemoglobinuria
Kematian bisa terjadi dalam 1 atau2 hari; jika penderita bertahan dari episode akut, maka tanda keracunan kronik dapat muncul.
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Keracunan Akut
Keracunan Kronis
(Plumbisme)
Gejala plumbisme dibagi ke
dalam 6 kategori :
1. pencernaan
2. neuromuskular
3. SSP
4. hematologik
5. ginjal
6. lain-lain
Efek pd Sal. Cerna Toksisitas lambung kadang mulai
dgn gejala seperti anorexia, kelainan otot, malaise, and
Rasa logam yang persisten muncul secara dini
Bila intoksikasi berlanjut, makaanorexia dan constipation menjadi lebih nyata
Spasme usus, yang menyebabkan nyeri perut yang parah (colic timbal),keadaan yang paling mencekam
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Efek Neuromuskular
• Sindroma neuromuskular (lead
palsy), ditandai dengan
kelemahan otot, terjadi lama
sebelum paralisis dan menjadi
satu-satunya gejala
Efek SSP
• Sindroma SSP (encephalopathy timbal) : manifestasi yang paling serius dari keracunan timbal, jauh lebih banyak terjadi pada anak-2 daripada org dewasa
• Tanda-tanda awal : kaku, vertigo, ataxia, sakit kepala, insomnia, gelisah, dan irritability
Efek Hematologik
• Anemia mikrositik hipokromik, lebih sering teramati pada anak2, secara morfologik serupa dengan akibat defisiensi besi
• Anemia ini diperkirakan karena dua faktor :
1. penurunan daya hidup eritrosit
2. penghambatan sintesis heme.
Efek pd GinjalToksisitas pd ginjal terjadi dlm dua bentuk :
1. Gangguan tubular reversibel (biasanya terlihat setelah pemaparan akut anak-anak pada timbal)
2. Nefropati interstisial ireversibel (lebih umum diamati pada pemaparan timbal industri jangka panjang
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Other Effects Pucat pada wajah
Kelu lidah
Gangguan retina
Penampilan penuaan dini "premature aging," with stooped posture, poor muscle tone, and emaciation;
black, grayish, or blue-black so-called lead line along the gingival margin
Lead also interferes with vitamin D metabolism
decreased sperm count
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Treatment of Lead Poisoning Chelation therapy is indicated in symptomatic
patients or in patients with a blood lead concentration in excess of 50 to 60 mg/dl (about 2.5 mM)
Four chelators :
1. edetate calcium disodium (CaNa2EDTA),
2. dimercaprol (British anti-Lewisite; BAL),
3. D-penicillamine,
4. succimer (2,3-dimercaptosuccinic acid; DMSA; CHEMET)
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MERCURY
Mercury was an important constituent of drugs for centuries as an ingredient in many diuretics, antibacterials, antiseptics, skin ointments, and laxatives
There have been epidemics of mercury poisoning among wildlife and human populations in many countries
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Chemical Forms and Sources of Mercury
three major chemical forms
1. mercury vapor (elemental mercury),
2. salts of mercury,
3. organic mercurials
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Minamata disease caused by methyl mercury (an organic mercury) Minamata is a small town in Japan, a chemical plant
empties its effluent directly into Minamata Bay The plant used inorganic mercury as a catalyst, and
some was methylated before entering the bay
the compound is then taken up rapidly by plankton algae and is concentrated in fish via the food chain
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Chemistry and Mechanism of ActionMercury readily forms covalent bonds with sulfur,
accounts for most of the biological properties of the metal
If sulfur is of sulfhydryl groups, divalent mercury replaces the hydrogen atom to form mercaptides, X-Hg-SR and Hg(SR)2, where X is an electronegative radical and R is protein.
Organic mercurials form mercaptides of the type R-Hg-SR’ capable to inactivate sulfhydryl enzymes so interfering with cellular metabolism and function
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Elemental Mercury Short-term exposure to vapor of elemental mercury may
produce symptoms within several hours :
weakness
chills
metallic taste
nausea
vomiting
diarrhea
dyspnea
cough
feeling of tightness in the chest
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Elemental Mercury Chronic exposure to mercury vapor produces a
more insidious form of toxicity that is dominated by neurological effects
continued exposure to mercury vapor develop psychological changes consist of depression, irritability, excessive shyness, insomnia, reduced self-confidence, emotional instability, forgetfulness, confusion, impatience, and vasomotor disturbances
Common features of intoxication from mercury vapor are severe salivation and gingivitis
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Organic Mercurials Symptoms of exposure to methylmercury are mainly
neurological
visual disturbance
ataxia
paresthesias
neurasthenia
hearing loss
dysarthria
mental deterioration
muscle tremor
movement disorders
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ARSENIC Arsenic is found in soil, water, and air as a common
environmental toxicant
The major source of occupational exposure to arsenic-containing compounds is from the manufacture of arsenical herbicides and pesticides
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Chemical Forms of Arsenic arsenic atom exists in the elemental form and in
trivalent and pentavalent oxidation states
toxicity increases in the sequence of organic arsenicals < As5+ < As3+< arsine (AsH3)
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Mechanism of Action Arsenate (pentavalent) is a well-known uncoupler of
mitochondrial oxidative phosphorylation
The mechanism is related to competitive substitution of arsenate for inorganic phosphate in the formation of adenosine triphosphate, with subsequent formation of an unstable arsenate ester that is rapidly hydrolyzed (arsenolysis)
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Toxicological Effects of Arsenic Cardiovascular System
Gastrointestinal Tract
Kidneys
Skin
Nervous System
Blood
Liver
Carcinogenesis and Teratogenesis
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