Anti-HSP70 monoclonal antibody, clone O38G45 [PE]

Lead tops the list of developmental toxicants released by industry into the environment according to Commission for Environmental Corporation.Hydrilla verticillatais an aquatic weed and rich source of variable nutrients and chemical constituents like saponins, vitamins, minerals, antioxidants, amino acids, detoxifying agents, etc. This weed is used in a beneficial way to detoxify lead in fish model. The fish were treated with sublethal concentration of lead to induce liver damage and fed with supplementary feed containing 20% of hydrilla dry powder. The present work revealed that lead accumulation is highly toxic to liver. Lead toxicity increased the expressions of cytochrome P450 1 A (CYP1A) and cytochrome P450 3 A (CYP3A) when compared to control. The metal binding stress proteins, heat shock proteins (Hsp60 & Hsp70) and metallothionein were also upregulated due to lead toxicity. Lead intoxicated fish exhibited reduced delta-aminolevulinic acid dehydratase activity in the blood, leading to reduced red blood cell count and changes in cell morphology. The lead toxicity also decreases the level of liver marker enzymes alanine transaminase, aspartate transaminase in serum. In hydrilla supplemented protective group, there was amelioration of these changes. Administration of supplementary feed to the lead intoxicated protective group significantly decreased the expressions of CYP1A, CYP3A, Hsp60, Hsp70 and metallothionein genes. The red blood cell count in lead intoxicated fish was maintained almost normal due to the protective action ofHydrilla verticillatain the diet. The observed increase in the enzymes, which further confirmed the protective effect ofHydrilla verticillataagainst lead induced toxicity.

Although the exact pathophysiology of critical illness polyneuropathy (CIP) is still unknown, there are several hypotheses, some of which are increased inflammation and oxidative stress. We used rodent sepsis model in which we induced sepsis through cecal ligation followed by cecal puncture. We then administered ascorbic acid (AA) and evaluated outcomes. The levels of malondialdehyde (MDA), tumor necrosis factor alpha (TNF-alpha), interleukins (IL)-6 in the plasma, and heat shock protein-70 (HSP-70) levels in the sciatic nerve were measured, and also electromyography analyses were performed. While plasma MDA, TNF-alpha, and IL-6 levels were decreased significantly with AA treatment, sciatic nerve levels of HSP-70 were significantly elevated in the AA group. A significant increase in compound muscle action potential (CMAP) amplitude and a significant decrease in CMAP latency were detected in the AA group. We observed healing effects of AA on a rat model of CIP and these effects seem to be related to its anti-inflammatory and antioxidant properties.