Calendula officinalis Linn. commonly known as marigold has long history of usage by the folklore system. It has a high economic value as herbal medicine and is widely used in cosmetics, perfumes, dyes, pharmaceutical preparations and food products for centuries. The plant has been approved for food use and appears in the food and drug administration (FDA) list of generally recognized as safe (GRAS) substances. The literature available for the comprehensive review study were taken from the different worldwide accepted scientific database, journals, books for botanical description, pharmacological properties and ethno-botanical uses of C. officinalis Linn. Natural products containing calendula either as extract or oil are complex mixtures containing hundreds of biologically active constituents such as carotenoids, flavonoids, saponins, sterols, phenolic acids, lipids, amino acids, carbohydrates, etc. These phytoconstituents have wide applicability in food and cosmetic industries besides their therapeutic applications viz. as antioxidant, antimicrobial, anti-inflammatory, anti-ulcer, anti-proliferative, antiparasitic, hypoglycemic, hypolipidemic and wound healing potential in experimental and clinical trials. Being useful therapeutic agents in their own right, an understanding of these traditional medicines has provided new plant derived drug leads to modern medicine for therapeutic application.

Plants have been used for thousands of years as medicine for treating variety of diseases and medical complaints by most of the civilizations. Juniperus communis L. is an evergreen aromatic shrub with high therapeutic potential for the treatment of diseases in human and animals. The plant is rich in aromatic oils, invert sugars, resins, catechin, organic acid, terpenic acids, leucoanthocyanidin, alkaloids, flavonoids, tannins, gums, lignins, wax, etc. Juniper berries or extract of the plant has traditionally been used as diuretic, anti-arthritis, anti-diabetes, antiseptic as well as for the treatment of gastrointestinal and autoimmune disorders. The essential oil and extracts of juniper have been experimentally documented to have antioxidant, antibacterial, antiviral and antifungal activities. Recent studies have also found anti-inflammatory, cytotoxic, hypoglycemic and hypolipidemic effects of berries in experimental models. Further, the essential oil incorporation retarded lipid peroxidation in preserved meat due to its high antioxidant effect which not only improved meat product quality but also improved shelf life of the product. Thus natural antioxidant such as juniper can be used in place synthetic antioxidant for the preservation and improving self-life of meat products. New well designed clinical trials in human and animals using well-characterized J. communis extract or oil need to be conducted so that additional information is generated which can support the use of this natural product as a nutraceutical.

The current study investigated the effects of deltamethrin, fluoride (F(-)) and their combination on the hepatic oxidative stress and consequent alterations in blood biochemical markers of hepatic damage in rats. Significant hepatic oxidative stress and hepatic damage were observed in the toxicant exposed groups. These changes were higher in the deltamethrin-F(-) co-exposure treatment group, depicting a positive interaction between the two chemicals.

The aim of the study was to investigate the ameliorative properties of ascorbic acid against the subchronic effect of co-exposure of fluoride (F) and chlorpyrifos (CPF) on oxidative damage markers such as lipid peroxidation (MDA) and antioxidant defense system in the liver of adult Wistar rats. The animal groups were provided with either vehicle or ascorbic acid (60 mg/kg, b.w.) or NOAEL dose of fluoride (1 ppm) or CPF (1 mg/kg, b.w.) or ten times of such doses orally alone and in combination or pre-treated with ascorbic acid along with co-exposure of F and CPF every consecutive day for 28 days. Hepatic damage marker analysis in blood revealed that aspartate and alanine aminotransferases, alkaline phosphatase, and lactate dehydrogenase were significantly (P < 0.05) increased with single or combined exposure of F or CPF at either dose levels. Significant increased oxidative damage of hepatocytes as indicated by increased MDA levels with decrease in tissue ascorbate and free radical scavenging enzymes like catalase, superoxide dismutase, and glutathione peroxidase was observed in groups treated with either F or CPF as well as in combinedly treated animals as compared to control animals. Supplementation of ascorbic acid restored the hepatic specific marker enzymes in blood following co-exposure of F and CPF at lower doses which were otherwise increased in the F and CPF co-exposed rats. The results show that ascorbic acid supplementation with F and CPF prevents or diminishes the hepatic damage in rats co-exposed to toxicants and may act as a putative protective agent against toxicant-induced liver tissue injury.

The present study was aimed to determine the total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI) of plasma and renal tissue in cisplatin (cDDP) induced nephrotoxic rats and its protection by treatments with floral extracts of Calendula officinalis Linn. Treatment with cDDP elevated (p < 0.05) the levels of blood urea nitrogen, creatinine (CR), TOS, OSI and malondialdehyde (MDA) but lowered (p < 0.05) total plasma proteins, TAS, total thiols (TTH), blood glutathione (GSH) and antioxidant enzymes compared to the control group. Pre- and post-treatments of ethanolic floral extract of C. officinalis along with cDDP restored (p > 0.05) CR, albumin, TOS, GSH and activities of antioxidant enzymes in blood and renal tissue. Ethanolic extract treatments reduced (p < 0.05) MDA level in renal tissue without restoring the erythrocyte MDA level following cDDP treatment. These observations were further supported by the histopathological findings in renal tissue. Observations of the present study have shown that treatments with ethanolic floral extract of C. officinalis protect cDDP induced nephrotoxicity by restoring antioxidant system of the renal tissue.

Fluorosis or crippling disease is one of the existing environmental challenges for animal and human beings in most parts of the globe. In the present study, sodium fluoride alone and with aluminium sulphate (ameliorative agent) was administered orally daily for 30 days in healthy goats of group 1 and 2, respectively, to access the effect on the electrocardiogram. All waves of Lead I, Lead II, Lead III, aVR, aVL and aVF in electrocardiographs were recorded before and after 30 days exposure of fluoride. A significant (P < 0.05) increase in P-R, Q-T and S-T intervals were observed in goats of group 1 as compared to their pre treatment values. The T wave duration was also significantly (P < 0.05) prolonged and as a result, bradycardia was observed after subacute exposure of fluoride for 30 days in group 1. But, in group 2, no such changes were observed. On the basis of results, it may be concluded that subacute toxicity of fluoride produces significant changes in different waves of electrocardiogram and aluminium sulphate has ameliorative efficacy.

BackgroundIt is an established fact that humans and animals are exposed to more than one chemical concurrently from various sources such as food, air and water. In the past, much emphasis was laid on evaluating the toxic effects of a single chemical. Nowadays an increased attention is being paid to the interaction of xenobiotics with one another. Therefore, a study was aimed to evaluate the potentiating effect of imidacloprid (IMI) on arsenic-induced testicular toxicity in rats.MethodsAdult male Wistar rats randomly divided into eight groups with six in each were subjected to daily oral administrations for 28 days. Group I served as control, group II received IMI at the dose rate of 16.9 mg/kg body weight, group III, IV and V received arsenic at the dose rate of 50, 100 and 150 ppb in drinking water whereas group VI, VII and VIII received both arsenic and IMI.ResultsRepeated oral administrations of IMI or arsenic (150 ppb) alone resulted in a significant (P < 0.05) elevation in the levels of malondialdehyde (MDA) and advanced oxidation protein product (AOPP) along with significant (P < 0.05) decline in total thiols and antioxidant enzymatic activities indicating reduced antioxidant defense in testicular tissue of exposed rats. These findings were further corroborated with histological alterations in testes like fluid accumulation in interstitial spaces in IMI administered rats. Similarly, rats provided access exclusively to arsenic-containing drinking water induced degenerative changes in seminiferous tubules in a concentration-dependent manner. Concurrent administration of IMI and arsenic produced more severe antioxidant and histopathological alterations of testes as compared to exposure to either toxicant.ConclusionsReduced antioxidant activities, increased MDA and AOPP levels with severe histopathological alterations in testes of rats on concurrent exposure indicated that IMI potentiated the arsenic-induced testicular toxicity in Wistar rats.

The study evaluated the effect of commercial preparation of deltamethrin, Butox, and fluoride (F) co-exposure on the brain antioxidant status and cholinesterase activity in rats. Group A was untreated. Group B was gavaged Butox, providing deltamethrin at the dose rate of 1.28 mg per kg body weight per day. Group C was administered F, as NaF, in drinking water providing 20 ppm F. Group D received both deltamethrin and F at the same dosages as groups B and C, respectively. Although, glutathione S-transferase activity was induced only in Butox alone treated group, the activities of superoxide dismutase and catalase were inhibited in all treatment groups when compared to the control group. Elevated lipid peroxidation was observed in the groups exposed to F. The activity of erythrocyte acetylcholinesterase (AChE) was inhibited in Butox treated groups, whereas brain AChE activity was inhibited in all treatment groups. In conclusion, both deltamethrin (given as Butox) and F inhibit AChE activity and produce oxidative stress in brain with F producing more oxidative damage. However, compared to the individual exposures, the co-exposure of these chemicals does not produce any exacerbated alteration in these biochemical parameters.