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

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