The present investigation was carried out to examine the cytotoxic and genotoxic effects of a Tinospora cordifolia crude methanolic extract (palmatine) on human skin epithelial carcinoma cells (A431). T. cordifolia is one of the indispensable medicinal plants used in Ayurvedic medicine for treatment of various diseases and recommended for improving the immune system. Cytotoxicity and genotoxicity evaluation was carried out using A431 cells treated with different concentrations of palmatine. The duration of the treatment was 24 and 48 hr.

Boswellia papyrifera and Boswellia carterii diffuses smoke polluting air that adversely affects indoor environment that certainly harm human health. Therefore, this study aims at ascertaining the effect of these plants on gonadal hormones and molecular changes in rat spermatozoa. The animals were exposed to 4 g/kg body weight of B. papyrifera and B. carterii daily for 120 days along with suitable controls. Significant decreases in FSH, LH and testosterone levels were evidenced, along with a reduction of protein, sialic acid, and carnitine levels.

Nickel nanoparticles (NiNPs) are increasingly used in various applications due to their unique properties. However, there is little information concerning the toxicity of NiNPs in the human skin cell (A431). The present study was designed to investigate the cytotoxicity, apoptosis, and DNA damage due to NiNPs in A431 cells. A cellular proliferative capacity test showed that NiNPs induce significant cytotoxicity in a dose- and time-dependent manner.

 Silver is one of the most toxic metals to freshwater aquatic organisms. Limited efforts have been made to study apoptosis and genotoxic potential of silver nanoparticles (AgNPs) in freshwater snail Lymnea luteola L. (L. luteola).

Iron oxide (Fe3O4) nanoparticles (IONPs) have received much attention for their utility in biomedical applications such as

This study monitors and assesses the effect of battery-manufacturing effluent containing metals Pb, Zn and Cd
on endogenous antioxidants. Malonaldehyde (MDA), reduced glutathione sulfyhydryl (GSH) and catalase (CAT)
which are known biomarkers of effluent were exposed to 0%, 25%, 50%, 75% and 90% amendments for 74h on
the gills, liver and kidneys of C. punctata. There was more metal Zn accumulation in the gills and GSH contents
increased significantly in the gills (P<0.01), liver accumulation of Pb was found to be more (P<0.05), whereas lowest

Increasing use of nickel oxide nanoparticles (NiO NPs) necessitates an improved understanding of their potential impact on human health. Previously, toxic effects of NiO NPs have been investigated, mainly on airway cells. However, information on effect of NiO NPs on human liver cells is largely lacking. In this study, we investigated the reactive oxygen species (ROS) mediated cytotoxicity and induction of apoptotic response in human liver cells (HepG2) due to NiO NPs exposure. Prepared NiO NPs were crystalline and spherical shaped with an average diameter of 44 nm.

Background: Arsenic is a ubiquitous environmental toxicant, and abnormalities of the skin, lung, kidney, and liver are the most common outcomes of long-term arsenic exposure. This study was designed to investigate the possible mechanisms of genotoxicity induced by arsenic trioxide in human hepatocellular carcinoma cells. Methods and results: A mild cytotoxic response of arsenic trioxide was observed in human hepatocellular carcinoma cells, as evident by (3-(4,5-dimethyl thiazol-2-yl)-2, 5-diphenyl tetrazolium bromide) and lactate dehydrogenase assays after 24 and 48 hours of exposure.

The wide scale use of copper oxide nanoparticles (CuONPs) due to their unique properties and important applications in magnetic, thermal, electrical, sensor devices, and cosmetics makes human beings more prone to the exposure of CuONPs and its potential adverse effects. Exposure to such nanoparticles is mainly through skin and inhalation. Therefore, the aim of the present study was to assess the apoptotic and genotoxic potential of CuONPs (50 nm) in the human skin epidermal (HaCaT) cells and its underlying mechanism of cellular toxicity.