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Parasitization of silkworm,  Bombyx mori  by invasive larva of dipteran parasitoid  Exorista bombycis  caused upto 20% revenue loss in sericulture. The parasitism was successful by suppressing host immune system however mechanism of immune suppression induced by  E. bombycis  is unknown which is unravelled here. The infestation induced cytotoxic symptoms in host hemocytes, such as vacuolated cytoplasm, porous plasma membrane, indented nuclei with condensed chromatin and dilated RER. One of the markers of necrosis is cell permeabilization, which can be measured as released lactate dehydrogenase (LDH). LDH level showed significantly ( P &lt;0.01) high release into extracellular medium  in vitro  after exposure of hemocytes to parasitoid larval tissue protein compared with control revealing membrane permeability and loss of cell integrity. At five minutes after exposure, cytotoxicity was 43% and was increased to 99% at 3h. The cytotoxicity is signalled by increased content of hydrogen peroxide (H 2 O 2 ) causing lipid peroxidation followed by porosity in plasma membrane. A test for lipid peroxidation by measurement of lipid peroxidation breakdown product, malondialdehyde (MDA) revealed significant increase in peroxidation from one to 24 h post-invasion, with maximum at 12 h ( P &lt;0.008). Level of reactive oxygen species measured as H 2 O 2  production increased from 6 to 12 h post-invasion and continued to increase significantly ( P &lt;0.03) reaching maximum at 48 h. These observations reveal that dipteran endoparasitoid invasion induced H 2 O 2  production in the hemocytes causing cytotoxicity, lipid peroxidation and membrane porosity that suppressed both humoral- and cell-mediated immune responses of hemocytes in  B. mori .

acta parasitologica

Oxidative stress and cytotoxicity elicited lipid peroxidation in hemocytes of  Bombyx mori  larva infested with dipteran parasitoid,  Exorista bombycis