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Aflatoxin
Aflatoxin is a metabolic product of Aspergillus flavus although there are claims of production of aflatoxin-like substances by other Aspergillus and Penicillium spp.
Aflatoxin attracted the attention of microbiologists in the United Kingdom in 1960 when countless turkeys and ducks died due to contamination of their feed of groundnut cakes with Aspergillus flavus. The disease manifestation in infected turkeys was due to the damage caused to the liver and kidneys of the animals by aflatoxin. Since this initial outbreak of the turkey-disease, considerable work has been done on the biochemical and microbiological aspects of aflatoxin and it is now known
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Inhibition of cell wall synthesis by penicillin |
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| (A) Bacterial Cell wall |
(B) Penicillin |
(C) Cell wall Precursors |
(D) Cross Linked |
| (E) Carboxypeptidase |
(F) Cell membranes |
(G) Porins |
(H) Autolysins |
| (I) Cytoplasm |
(J) Cross Linkage Disruption |
(K) Cell wall turgidity |
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The inhibition of cell wall synthesis by penicillin: Normally, as shown in the left side of the figure, cell wall precursors (C) are cross-linked (D) by specific enzymes, transpeptidases and carboxypeptidases, also known as penicillin binding proteins (E) in the cell membranes (F) and then added on to the growing bacterial cell wall (A). However, when penicillin (B) gets into the cell through porins (G) as shown in the right side of the figure, the antibiotic binds to the specific enzymes (E). This leads to the release of autolysins (H) by the cell membrane (F) into the cytoplasm (I). The autolysins (H) prevent the cell wall precursors (C) to form cross linkage leading to their disruption (J) and lack of participation in cell wall growth which ultimately leads to a loss in cell wall turgidity (K) and death of the bacterial cell
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Inhibition of steps involved in protein synthesis by tetracyclines |
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| (A) Antibiotic Tetracycline |
(B) Porins |
(C) Cell Wall |
| (D) Cytoplasmic Membrane |
(E) Cytoplasm |
(F) Ribosomal sub-unit |
| (G) mRNA |
(H) tRNA |
(I) Deformed Protein |
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Inhibition of steps involved in protein synthesis by tetrayclines: The antibiotic tetracycline (A) enters bacteria through porins (B) in the cell wall (C) and is actively transported across cytoplasmic membrance (D). In the cytoplasm (E), the antibiotic binds to 30S ribosomal sub-unit (F) of mRNA (G) causing misreading of tRNA (H) leading to deformed protein (I). that aflatoxin consists of several chromatographically distinguishable components like aflatoxin B1, B2, G1, G2, M1, M2, etc.
Afaltoxins are known to posses carcinogenic properties and mainly affect animals such as birds, fish, cattle, swine, sheep, goats, dogs and monkeys. Human beings are rarely affected by aflatoxin unless large quantities of groundnut infested by A. flavus are consumed.
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Reports are available which imply the accumulation of considerable amounts of aflatoxin in the breast milk of mothers fed on preparations made from moldy grains. Experimental production of aflatoxins by inoculation with A. flavus has been reported in several agricultural commodities such as copra, wheat, rice, cotton, oats, groundnut, corn and cloves. There appears to be some degree of strain specificity in aflatoxin production, since certain isolates produce abundant toxin while others do not. Surveys of domestic grains for aflatoxin levels by official grain standards of the U.S.A. showed that incidence of the toxin in sorghum could be as low as 3-6 mg/kg seed while com had levels reaching 13-15 mg/kg. Root crops such as cassava and sweet potato, coffee and forage crops have been found to be contaminated with aflatoxin. High humidity during harvest and improper methods of post-harvest drying are prime factors. contributing to the infestation of grains by aflatoxin producing aspergilli.
There are also several reports on the effects of aflatoxin on higher plants. The effects include inhibition of seed germination, induction of chlorophyll deficiency, mitochondrial injury, interference with nucleic acids especially messenger RNA and inhibition of various enzyme systems. The toxin inhibits the growth of Rhizobium in vitro and root nodulation of cluster clover (Trifolium glomeratum) seedlings grown on agar slopes. It also induces the formation of nodule-like outgrowth on the root system even in the absence of Rhizobium.
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