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TOKSISITAS LOGAM BERAT

PENDAHULUAN 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

TOKSISITAS LOGAM BERAT


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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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
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.

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, maka anorexia dan constipation menjadi lebih nyata Spasme usus, yang menyebabkan nyeri perut yang parah (colic timbal), keadaan yang paling mencekam

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 Neuromuskular Sindroma neuromuskular (lead palsy), ditandai dengan kelemahan otot, terjadi lama sebelum paralisis dan menjadi satu-satunya gejala

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 Ginjal
Toksisitas 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

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

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 Action


Mercury 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 arseniccontaining compounds is from the manufacture of arsenical herbicides and pesticides

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Chemical Forms of Arsenicin arsenic atom exists in the elemental form and
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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