Hemotoxicity

Hemotoxic venoms of rattlesnakes and cottonmouths contain as their principal toxin phosphodiesterase, an enzyme that catalyzes hydrolysis ofphosphodiester bonds in ATP and other substrates. 

Hemotoxic activity. Seed oil, administered orally to human adults, produced thrombocytosis in children, the effect was inactivated by ultraviolet radiation . Hypercholesterolemic activity. Seed oil, administered by gastric intubation to rabbits at a dose of 0.4 g/kg, was inactive " . Male Wistar rats fed 12 or 24% sesame oil in the diet for 4 weeks were investigated. The rats on the 24% sesame oil diet had significantly lower lymphatic cholesterol and fatty acids . 

Hemotoxic. Poisonous to the blood and hematopoietic system (system pertaining to or effecting the formation of blood cells). Hepatectomy. Removal of a part of the liver. 

Bowman ZS, Morrow JD, JoIIow, DJ, et al. Primaquine induced hemolytic anaemia role of membrane lipid peroxidation and cytoskeletal protein alterations in the hemotoxicity of 5-hydroxyprimaquine. J Pharmacol Exp Ther 2005 314 838-845. 

Although hemotoxicity was not observed during premarketing studies of olanzapine (202), cases of neutropenia (neutrophil count below 1.5 x 109/1) (203) or agranulocytosis (neutrophil count below 0.5 x 109/1) (204) have been published. 

The authors of the second case stated that, in spite of decades of experience with haloperidol, an associated literature search has revealed only very rare instances of hemotoxicity, and since lorazepam is not known to cause leukopenia, olanzapine may have been the more likely offender the simultaneous effect of both antipsychotic drugs, olanzapine and haloperidol, is unknown. 

SAFETY PROFILE Suspected carcinogen with experimental carcinogenic data. A human poison by inhalation. Human systemic effects by inhalation anorexia, nausea or vomiting. Corrosive to skin can produce severe burns. Human mutation data reported. A powerful fumigant gas that is one of the most toxic of the common organic halides. It is hemotoxic and narcotic with delayed action. The effects are cumulative and damaging to nervous system, kidneys, and lung. Central nervous system effects include blurred vision, mental confusion, numbness, tremors, and speech defects. 

Even the normal dose of sodium stibogluconate can lead to both cardiotoxicity and hemotoxicity, because of its cumulative effects. 

Because of hepatotoxicity and carcinogenicity (hepatoma) detected in preclinical studies, and hemotoxicity and gastrointestinal adverse effects in man, diftalone has been withdrawn by its manufacturer (1). 

The kinetics of the hemotoxic effects of interferon alfa have been studied in 76 patients with chronic hepatitis C (210). There were significant falls in white blood ceU count and platelet count within 12 hours after the first injection, and a second fall in platelet count after 2 weeks, but not further thereafter. This rapid time-course suggests that liver or spleen sequestration of blood cells, rather than direct bone marrow suppression or immune-mediated hematological toxicity, is the most likely explanation for this acute hemotoxic effect, which does not preclude continuation of treatment. 

Isolated anemia is not a common feature of the hemotoxic effects of interferon alfa, and pure red cell aplasia has been reported in two patients with chronic leukemia for several months (217,218). Both patients improved progressively after replacement of interferon alfa by hydroxyurea. However, one required erythrocyte transfusions for 14 months. 

Synergistic hemotoxicity has sometimes resulted from the combination of interferon alfa with zidovudine in AIDS-associated Kaposi s sarcoma, but this regimen is considered to be relatively safe (421,422). 

Dornsife RE, Averett DR. In vitro potency of inhibition by antiviral drugs of hematopoietic progenitor colony formation correlates with exposure at hemotoxic levels in human immunodeficiency virus-positive humans. Antimicrob Agents Chemother 1996 40(2) 514-19. 

In a 46-year-old man taking olanzapine 10 mg/day, leukopenia and neutropenia were associated with HLA types A1 24, B7, B35, DRB1 15, DRB1 11, DRB3 01-03, DRB5 01-02, a haplotype distinct from that previously observed in clozapine-induced hemotoxicity (148). 

Lauwerys R, Bernard A, Viau C, Buchet JP. Kidney disorders and hemotoxicity from organic solvent exposure. Scan J Work Environ Health 1985 II (suppll) 84-90. 

Snake venoms are complex mixtures of several different components or fractions that can vary considerably within Crotalinae members. A complete review of venom components is beyond the scope of this review. Depending on the content of the venom, multiple organ systems may be affected. Historically, Crotalinae venom was classified as neurotoxic, hemotoxic, cardiotoxic, or myotoxic, depending on the species of snake involved in the envenomation. This oversimplifies the complex nature of Crotalinae venom. Clinically, a patient may develop such multisystem disorders as platelet destruction, internal bleeding, hypotension, paresthesias, and rhabdomyolysis. 

Experimental design Young (4-5 weeks) and adult (9-13 weeks, 5-6 months, and 16 months) rats were dosed with 0, 32, 63, 125, 250, or 500 mg/kg 2-butoxyethanol by gavage. Hemotoxicity and metabolism and excretion of 2-butoxycthanol was monitored for 48 hours. Animals were killed at 24 and 48 hours after treatment and spleen, liver, kidney, testes, and urinary bladder were weighed, fixed, and examined. Histopathological results were presented for the control, 125, 250, and 500 mg/kg dose group. 

Clinical manifestation. It includes several syndromes a) pulmotoxic and irritative syndrome - expressed by catarrhal changes on the contact mucosa and respiratory tract, toxic pulmonary oedema b) hemotoxic syndrome - expressed by severe hemolysis of different degrees, in the severe forms - hemolytic shock and anaemia c) hepatal syndrome - characterised by subicterus or icterus, increased liver and bilirubinaemia d) renal syndrome - by oliguria or anuria, pathological deviations in the urine and acute kidney insufficiency. In the extremely severe forms consciousness is disordered. Laboratory blood and urine chemical tests show evidence of phenol metabolites, data for blood damage (increased values of free hemoglobin, reduced number of erythrocytes), positive liver tests etc. 

Damaging processes. The organism is injured by the hemotoxic processes - hemoglobinaemia and severe hemolysis with shock fits, neural, liver and kidney cells metabolism disorders occur. A mild irritative effect on the contact mucosa is also observed. 

Clinical manifestation. It includes the following syndromes a) irritative-pulmotoxic syndrome - with evidence of catarrhal tracheobronchitis, combined with toxic oedema in the severe cases b) cerebral toxic syndrome characterised by ataxia, Menier s syndrome, the severe forms manifest disordered consciousness c) hepatotoxic syndrome - observed in the extremely severe cases of poisoning, manifested as icterus, hepotomegalia and increased blood bilirubin and transaminase values sometimes it is manifested as hepatorenal syndrome d) hemotoxic syndrome - rarely met in acute intoxication by methemoglobinaemia, hemolysis, leukopoenia. 

I. Mechanism of toxicity. Snake venoms are complex mixtures of 50 or more components that function to immobilize, kill, and predigest prey. In human victims, these substances produce local digestive effects on tissues as well as hemotoxic, neurotoxic, and other systemic effects. The relative predominance of digestive, hemotoxic, or neurotoxic venom components depends on the species of the snake and geographic variables. 

Lerza RA, Bogliolo GV, Mecoboni MP, Saviane AG, PannacchiUi IM. Effect of H2 antagonists cimetidine and famotidine on the hemotoxicity of cyclophosphamide. Anticancer Res... 

Chitosan Have inherent antibacterial activity some members have been found hemotoxic whether chitosan polymers are totally biodegraded in an animal body is still not known. 

In some cases, the use of a membrane filterlike system but with a defined geometry can improve performance. Hosokawa et al. [8] developed an array of fuimel-Uke microcavities. RBCs are pumped through the cavities to waste, while the larger WBCs are trapped (Fig. 4). This was used to trap CD4+ cells and later used to study hemotoxicity in mouse leukocytes. 

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