2. Haematotoxicity
Hematotoxicity essentially affects two basic homeostatic
functions:
(1)RBC-mediated
oxygen transport
(2)
the production of red and
white blood cells
and platelets.
5. MOA of Haematotoxicity
RBC-mediated
oxygen transport fails
the production of red and
white blood cells & platelets.
HYPOXIA Bone marrow suppression
Tissue respiration impaired
Anaerobic Respiration
1) RBC: Oxygen transport fails
2) WBC: Impaired defence and
Immune system
3) Platelets: Impaired coagulation
mechanism
Acidosis & Cells damage
6. blood toxicities that were commonly encountered in
occupational settings such as
1. benzene-induced bone marrow suppression, Acute
Leukemia
2. aniline and nitrobenzene induced methemoglobinemia,
3. hydrogen sulfide–induced effects.
4. carbon monoxide (impairment of oxygen transport)
7. Exposure to hydrogen sulfide can be a significant industrial
concern in the refining of petroleum products and the
biological degradation of Grain, corn etc.
As for the number of workers affected, benzene and
hydrogen sulfide probably constitute the most significant
risk factors for toxicity
8. dapsone (used to treat leprosy) and primaquine (used to
treat malaria) can produce a fatal hemolytic anemia in
certain genetically predisposed individuals (those with a
deficiency in glucose-6-phosphate dehydrogenase).
13. Introduction:
The skin is the largest organ in the body and is continually
exposed to external stimuli, such as chemical and
environmental substances.
Cutaneous toxicity can be broadly classified according to
the mechanism of onset, namely:
14. 1)Contact dermatitis:
damage resulting from
contact with a substance
(irritant dermatitis,
allergic contact
dermatitis, chemical
burns)
2)Photosensitivity:
caused by combined
effects of a substance &
ultraviolet light
(phototoxic dermatitis,
photoallergy contact
dermatitis);
3) Contact urticaria:
chemical-induced acne;
pigmentary disturbance;
drug rash;
hair disturbance;
nail disturbance; or
tumor-induced.
15.
16.
17.
18. Skin carcinogenesis
Some photoirritants, such as 8-methoxypsoralen, have
been associated with UV-induced skin carcinogenesis.
p53 is a protein that causes cell cycle arrest, apoptosis, or
senescence that is crucial in the process of tumor
suppression in several cell types
19. DMBA/TPA two-stage skin carcinogenesis model, the absence of p53 in
stratified epithelia leads to the appearance of a higher number of tumors that
grow faster and become malignant more frequently than tumors arising in
mice with the wild type p53 genotype