The fruits of Emblica officinalis (Amla) are widely used in the Indian System of Medicine and are believed to increase defense against disease. In the present study, the effects of chronic oral administration of fresh fruit homogenate of Amla on: (i). myocardial antioxidant system and (ii). oxidative stress induced by ischemic-reperfusion injury (IRI) in rat heart were investigated. Fresh amla fruit homogenate, in three different doses (250, 500 and 750 mg/kg) and normal saline (C) were administered orally to Wistar albino rats (120-150 gms) of either sex daily for 30 days. There was reduction in basal myocardial lipid peroxidation, as evidenced by decreased thiobarbituric acid reactive substances (TBARS) level, and augmentation of myocardial endogenous antioxidants, like superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) in the treated rats. Hearts were also subjected to in vitro IRI (9 min of global ischemia, followed by 12 min of reperfusion, Langendorff's mode). Significant myocyte injury and rise in myocardial TBARS along with depletion of SOD, catalase, GSH (reduced glutathione) and GPx occurred in the control group. No significant increase in myocardial TBARS and depletion of antioxidant enzymes were observed in the treated groups. Myocyte injury was evident only in 250 mg/kg group. The results indicate that chronic Emblica officinalis administration causes myocardial adaptation by augmenting endogenous antioxidants and protects rat hearts from oxidative stress associated with ischemic-reperfusion injury.

Iron oxide (Fe2O3) nanoparticles are widely used in different fields of nanotechnology. However, studies on its toxicological effects in humans and the environment are scarce. Therefore in this investigation 28 days repeated dose oral toxicity studies were conducted on Fe2O3-30 nanoparticles and its counterpart Fe2O3-Bulk with special reference to target biochemical enzymes and histopathological changes in different tissues of female albino Wistar rats. The alterations observed after Fe2O3-30 treatment in various tissues of exposed rats were dose dependent. Low dose was less effective than medium and high doses with low dose demonstrating "no observed adverse effect" (NOAEL). Further, high dose treated rats showed toxic sign and symptoms but no mortality. Due to the repeated doses of Fe2O3-30 nanoparticles, significant inhibition was observed in total, Na(+)-K+, Mg2+ and Ca(2+)-ATPases in brain of exposed rats. Similarly, significant inhibition was recorded in RBC and brain acetylcholinesterase indicating that both synaptic transmission and nerve conduction were affected by this compound. Fe2O3-30 significantly increased aspartate amino transferase, alanine amino transferase and lactate dehydrogenase in serum and liver, whereas, these enzymes were significantly decreased in kidney indicating tissue necrosis and possible leakage of these enzymes into the blood stream. Increased levels of these enzymes in liver as well as in serum might be an adaptive mechanism due to the stress of iron nanoparticles. High dose treated rats of Fe2O3-30 showed dilated central vein, perivascular round cell collections in liver along with focal areas of necrosis, whereas kidney showed focal tubular damage and red pulp congestion, whereas prominent white pulp indices were observed in spleen. However, histopathological analysis of heart and brain tissues failed to show any adverse changes in their architecture exposed to repeated doses of Fe2O3-30 when compared with controls. Fe2O3-Bulk did not induce any adverse effects in either biochemical parameters or histopathology in the treated rats and the changes observed were near to controls and mostly insignificant, indicating that the counter part of nanoparticles i.e., bulk material is less potent than the nanoparticles in causing toxicity in the exposed animals. These results suggested that as particle size decreases, this iron nanoparticle showed increased toxicity, even though the same material is relatively inert in bulk form. The changes observed in these target enzyme activities could be useful as biomarkers of exposure to nanoparticles.

Magnetic iron oxide nanoparticles with appropriate surface chemistry have been widely used with potential new applications in biomedical industry. Therefore, the aim of this study was to assess the size-, dose-, and time-dependent effects, after acute oral exposure to iron oxide-30 NP (Fe(2)O(3)-30), on various biochemical enzyme activities of clinical significances in a female Wistar rat model. Rats were exposed to three different doses (500, 1,000, and 2,000 mg/kg) of Fe(2)O(3)-30 and Fe(2)O(3)-Bulk along with control. Fe(2)O(3)-30 had no effect on growth, behavior, and nutritional performance of animals. Fe(2)O(3)-30 caused significant inhibition of acetylcholinestrase in red blood cells as well as in brains of treated rats. Further, more than 50% inhibition of total, Na(+)-K(+), Mg(2+), and Ca(2+)-ATPases activities, as observed in brains of exposed female rats, may be the result of disturbances in cellular physiology and the iono-regulatory process. Activation of the hepatotoxicity marker enzymes, aspartate aminotransferase and alanine aminotransferase, was recorded in serum and liver, whereas inhibition was observed in kidney. Similarly, enhancement of lactate dehydrogenase activity was observed in serum and liver; however, a decrease in enzyme levels was observed in kidneys of Fe(2)O(3)-30-treated rats. On the other hand, Fe(2)O(3)-Bulk did not depict any significant changes in these biochemical parameters, and alterations were near to control. Therefore, this study suggests that exposure to nanosize particles at acute doses may cause adverse changes in animal biochemical profiles. The use of the rat model signifies the correlation with the human system.

Withania somnifera is an important medicinal plant, however, its cultivation and quality are compromised through infestation by leaf spot disease caused by the fungus, Alternaria alternata. To find suitable strategies against this disease, studies on postinfectional changes are important. ROS are critical as they interact with other defence signalling pathways. We analyzed ROS-generating and scavenging systems in healthy and diseased leaf samples of W. somnifera and ROS-driven downstream defence pathways.• We used DAB and NBT assays for ROS detection, spectrophotometry and in-gel assays for ROS scavenging enzymes, a thioglycolic acid (TGA) based assay, histochemical staining for lignin, and qRT-PCR for transcript-level expression.• Leaf spot infection in W. somnifera increased NADPH oxidase activity and ROS accumulation in infected leaves, together with enhanced antioxidant enzyme activity. Leaf spot-infected leaves had increased lignin content and higher expression of lignin biosynthesis genes. In addition, transcript levels of defence-related genes, NPR1 and PR, were also upregulated.• The present work provides insights into responses to leaf spot disease through defencerelated signalling in W. somnifera. It demonstrates crosstalk between ROS and lignin biosynthesis. This work identified potential targets for developing strategies to confer disease resistance against A. alternata in W. somnifera.