, Diagnosis an-&& of Shrimp Diseases - Central Institute of ...

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The liver is the major site of GSH synthesis in humans and animals.In the liver, itdetoxifies endogenous metabolic peroxides through glutathione peroxidase and of exogenoussubstances such as drugs and other xenobiotics through glutathione-S-transferase. GSHsynthesised in the hepatic cells is either translocated to plasma or excreted into the bilethrough carrier mediated transport. During infection and inflammatory processesGSH ismobilised from the liver to the pathological site.Decrease of hepatic thiols is due toincreased efflux of glutathione in shock induced inflammatory reaction.Regulation of cellular levels of GSH can be broadly divided into four areas (1) Uptakeof precursor aminoacids and intact GSH, (2) the regulation of the enzymes necessary forGSH synthesis, (3) alteration in the cellular redox system due to increased lipid peroxidationand cross-linking of glutathione with aldehyde, (4) direct oxidation of glutathione by ROS.Uptake of cysteine is the rate-limiting step for GSH synthesis.GSH also forms conjugated products with ingested toxins and provide a detoxifyingstep, the GSH conjugates show less toxicity and are easily excreted in the faeces and urine.Glutathione-S-transferase (GSTs) is inducible and has been found to be induced in rat liverwhen AFBl is ingested.Combating free radicals and their inactivationThe third line of defense is damage control which is achieved by providing freeradical scavengers and antioxidant enzymes.The former arrests the initiation andpropagation of the free radical chain reactions. They react rapidly with the free radicals,inactivate them and control the damage. While doing so the scavengers themselves areconverted to radicals, which are many times less toxic than the original free radical.Vitamin E ( a - tocopherol), Vitamin C (ascorbic acid) Vitamin A, !.3 - carotene and reducedglutathione are free radical scavengers and are considered as antioxidants. These free radicalscavengers interact as synergists and such interaction takes place at different levels, asdetailed below :-aAntioxidant regeneration - e.g. Vitamin E is regenerated by Vitamin Cb Protective mechanism - e.g. Vitamin E protects p-carotene fromautooxidationcCompensatory mechanism - e.g. Vitamin E ameliorates selenium deficiencyand vice versad. Complementary mechanism - e.g. p-Carotene may complement Vitamin E andprevent lipid peroxidation
AFB, induced ~nutagenesis in Salmonella is partially inhibited by the free radicalscavengers, vitamin analogues, Ascorbic acid and vitamin E. Vitamin E was more potentthan vitamin C in AFBl induced mutagenesis. Dietary selenium supplementation was foundto provide protection against AFB, induced neoplastic foci in rat liver.Antioxidant enzyme activitiesAntioxidant enzymes qe universally distributed in all the cells and combat ROS anddestroy them to prevent their interaction with cellular compounds. Superoxide dismutase(SOD) protects cells and tissues-from inflammatory damage by inactivating the superoxidefree radical.SOD20,-'H2022~'Catalase and glutathione peroxidase (GPx) act upon Hz02 and inactivate it. Both theenzymes have been detected in all human cells and organs with the highest activity inerythrocytes, liver and kidney.Catalase2H202 2H,O + 02GPxH202 + 2GSH 2H20 + GSSG (Oxidised glutathione)GPx is a selenium containing protein and can act not only on hydrogen peroxide butalso on lipid hydroperoxide and arrest lipid peroxidation process.
Page 5 and 6:
OVERVIEW OF STRATEGIES FOR PREVENTI
Page 7 and 8:
in harmonizing aquatic animal healt
Page 9 and 10:
SI-IRXMP DISEASES: GENEIL4L ASPECTS
Page 11 and 12:
quantitative level of pathogen is i
Page 13 and 14:
presence of prominent eosinophiiic
Page 15 and 16:
Disease affected the shrimps of all
Page 19 and 20:
BACTERIAL AND FUNGAL DISEASES OF SH
Page 21 and 22: Cause: The epibiotic bacteria stich
Page 23 and 24: PARASiTIC AND NON-INFECTIOUS IIISEA
Page 25 and 26: XOS-INFECTIOUS DISEASESNon-infectio
Page 27 and 28: INVESTIGATING SHRIMP DISEASES: OBSE
Page 29 and 30: lnay be a predisposing factor for b
Page 31 and 32: BACTERIOLOGICAL METHODSS.V. Alavand
Page 34 and 35: In place of ZMA, nutrient agar prep
Page 36 and 37: Interpretation: Positive reaction i
Page 38 and 39: Incubate at 37°C for 1-2 h.Examine
Page 40 and 41: Alkaligens: etc. are resistant. The
Page 42 and 43: Culture Media, Reagents and StainsC
Page 45 and 46: Differential characteristics of Vib
Page 47 and 48: Davidson's Alcohol Formatin Acetic
Page 49 and 50: Paraffin cold impregnationXylene an
Page 51 and 52: ProcedureDe-paraffinise the slid'c
Page 53 and 54: Biochemistry of Nucleic Acids with
Page 55 and 56: DNA e.rl1i6it.v base equivuleizcc!E
Page 57 and 58: hydrolyzed by dilute alkali. The su
Page 59 and 60: Polymerase Chain Reaction (PCR) is
Page 61 and 62: a number of viral, bacterial and pa
Page 63 and 64: from 15-30 bases. Negative controls
Page 65 and 66: PCR Primers for Indian WSVTwo sets
Page 67 and 68: ANTIOXIDANTS IN MANAGEMENT OF OXIDA
Page 69 and 70: Many potent chemical carcinogens ar
Page 71: cells. It has been shown that possi
Page 75 and 76: FIGURE 2. An overview of oxygen rad
Page 77 and 78: were responsible for production los
Page 79 and 80: for Asiatic region. The participati
Page 81 and 82: charge of the DNA fragment. The neg
Page 83 and 84: European countries have in place th
Page 85: irth to a new concept to treatment
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