Indirect Impacts of COVID-19 on the Environment: A Global Review.

Coronavirus (COVID-19) is an infectious disease caused by the SARS-CoV-2 virus, which has plagued the Earth for the past two years and brought much controversy along with it. This report aims to analyze how the Covid-19 pandemic has had indirect effects on the environment. The onset of the pandemic has not only caused havoc disrupting routine average and businesses, but also claimed at least five million lives worldwide. This prompted the governments and the World Health Organization (WHO) to formulate measures to contain the transmission and the impact of the disease on the populations. Quarantine measures, movement restrictions, lockdowns and curfews, and travel bans are some of the most effective response methods that have helped the world contain the pandemic's spread. The adopted measures have had an indirect impact on the environment, opening the global community to numerous opportunities and threats. This report provides a critical analysis of how the Covid-19 pandemic has had indirect effects on the environment, examining how the response and containment measures have affected the environment. It focuses on air quality, water demand and quality, climate change, afforestation and deforestation, wildlife resurgence, littering, traffic congestion, noise reduction and changed human activities. It explores how the Covid-19 containment measures have had an environmental impact with a keen interest in the earlier areas.

Biosynthesis of Silver Nanoparticles Using Azadirachta indica and Their Antioxidant and Anticancer Effects in Cell Lines.

In the present study, silver nanoparticles (Ag-NPs) were synthesized using Azadirachta indica extract and evaluated for their in vitro antioxidant activity and cytotoxicity efficacy against MCF-7 and HeLa cells. The silver nanoparticles (Ag-NPs) were formed within 40 min and after preliminary confirmation by UV-visible spectroscopy (peak observed at 375 nm), they were characterized using a transmission electron microscope (TEM) and dynamic light scattering (DLS). The TEM images showed the spherical shape of the biosynthesized Ag-NPs with particle sizes in the range of 10 to 60 nm, and compositional analysis was carried out. The cytotoxicity and antioxidant activity of various concentrations of biosynthesized silver nanoparticles, Azadirachta indica extract, and a standard ranging from 0.2 to 1.0 mg/mL were evaluated. The 2,2-Diphenyl-1-picrylhydrazyl (DPPH) activity of the biosynthesized Ag-NPs and aqueous leaf extract increased in a dose-dependent manner, with average IC50 values of the biosynthesized Ag-NPs, aqueous leaf extract, and ascorbic acid (standard) of 0.70 ± 0.07, 1.63 ± 0.09, and 0.25 ± 0.09 mg/mL, respectively. Furthermore, higher cytotoxicity was exhibited in both the MCF-7 and HeLa cell lines in a dose-dependent manner. The average IC50 values of the biosynthesized Ag-NPs, aqueous leaf extract, and cisplatin (standard) were 0.90 ± 0.07, 1.85 ± 0.01, and 0.56 ± 0.08 mg/mL, respectively, with MCF-7 cell lines and 0.85 ± 0.01, 1.76 ± 0.08, 0.45 ± 0.10 mg/mL, respectively, with HeLa cell lines. Hence, this study resulted in an efficient green reductant for producing silver nanoparticles that possess cytotoxicity and antioxidant activity against MCF-7 and HeLa cells.

Kolaviron ameliorates hepatic and renal dysfunction associated with multiwalled carbon nanotubes in rats.

The increase in the exposure to carbon nanotubes (CNTs) and their incorporation into industrial, electronic, and biomedical products have required several scientific investigations into the toxicity associated with CNTs. Studies have shown that the metabolism and clearance of multiwalled CNTs (MWCNTs) from the body involve biotransformation in the liver and its excretion via the kidney. Since oxidative stress and inflammation underlines the toxicity of MWCNT, we investigated the ameliorative effect of kolaviron (KV), a natural antioxidant and anti-inflammatory agent, on hepatorenal damage in rats. Exposure to MWCNTs for 15 days significantly increased serum activities of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and lactate dehydrogenase thereby suggesting hepatic dysfunction. Kidney function, which was monitored by urea and creatinine levels, was also impaired by MWCNTs. Additionally, MWCNTs markedly increased myeloperoxidase activity, nitric oxide level, reactive oxygen and nitrogen species, and tumor necrosis factor level in both tissues. However, KV in a dose-dependent manner markedly attenuated MWCNT-induced markers of hepatorenal function in the serum and MWCNT-associated inflammation in the liver and kidney. Also, MWCNTs elicited significant inhibition of superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase activities. There was a significant diminution in glutathione level (GSH) and enhanced production of malondialdehyde (MDA) in MWCNTs-exposed rats. KV treatment was able to significantly increase the antioxidant enzymes and enhance the GSH level with a subsequent reduction in the MDA level. Taken together, KV elicited ameliorative effects against hepatorenal damage via its anti-inflammatory and antioxidant properties. Thus, KV could be an important intervention strategy for the hepatorenal damage associated with MWCNTs exposure.

Correction to: Kolaviron via anti-inflammatory and redox regulatory mechanisms abates multi-walled carbon nanotubes-induced neurobehavioral deficits in rats.

After publication of this paper, the authors discovered that the name of the first author, Isaac Adegboyega Adedara, was missing in the proof. Dr. Adedara's intellectual contributions to the present article include conception and design of the study, manuscript writing and approval of the final version of the manuscript.

Kolaviron via anti-inflammatory and redox regulatory mechanisms abates multi-walled carbon nanotubes-induced neurobehavioral deficits in rats.

Exposure to multi-walled carbon nanotubes (MWCNTs) reportedly elicits neurotoxic effects. Kolaviron is a phytochemical with several pharmacological effects namely anti-oxidant, anti-inflammatory, and anti-genotoxic activities. The present study evaluated the neuroprotective mechanism of kolaviron in rats intraperitoneally injected with MWCNTs alone at 1 mg/kg body weight or orally co-administered with kolaviron at 50 and 100 mg/kg body weight for 15 consecutive days. Following exposure, neurobehavioral analysis using video-tracking software during trial in a novel environment indicated that co-administration of both doses of kolaviron significantly (p < 0.05) enhanced the locomotor, motor, and exploratory activities namely total distance traveled, maximum speed, total time mobile, mobile episode, path efficiency, body rotation, absolute turn angle, and negative geotaxis when compared with rats exposed to MWCNTs alone. Further, kolaviron markedly abated the decrease in the acetylcholinesterase activity and antioxidant defense system as well as the increase in oxidative stress and inflammatory biomarkers induced by MWCNT exposure in the cerebrum, cerebellum, and mid-brain of rats. The amelioration of MWCNT-induced neuronal degeneration in the brain structures by kolaviron was verified by histological and morphometrical analyses. Taken together, kolaviron abated MWCNT-induced neurotoxicity via anti-inflammatory and redox regulatory mechanisms.

A comparison of poly-ethylene-glycol-coated and uncoated gold nanoparticle-mediated hepatotoxicity and oxidative stress in Sprague Dawley rats.

BACKGROUND: Gold nanoparticles (GNPs) and their functional derivatives are of great interest because of their many biomedical applications. GNPs are increasingly being incorporated into new diagnostic and therapeutic approaches in medicine. Consequently, there has been a strong push to fully understand their interactions with blood components. The agglomeration of cells reflects the interaction of nanoparticles with blood components. METHODS: The main aim of this study was to compare the effects of poly-ethylene-glycol (PEG)-oated and uncoated GNPs on the generation of reactive oxygen species (ROS); on the actions of distinct hepatotoxicity biomarkers such as alanine (ALT) and aspartate (AST) aminotransferases, and alkaline phosphatase (ALP); and on the histology of liver tissues in the rat model. Four distinct doses of PEG-coated and uncoated GNPs (12.5, 25, 50, and 100 µg/kg body weight) were used. Each group consisted of three rats receiving an oral administration of PEG-coated and uncoated GNPs for 5 days with one dose per 24 hours. The control group consisted of three rats that received deionized water. Twenty-four hours after the last treatment, samples were collected following standard procedures. RESULTS: PEG-coated and uncoated GNPs enhanced the generation of ROS and the activity of serum aminotransferases (ALT/AST) and ALPs relative to the negative control. A liver histology assessment of GNP-exposed rats revealed statistically significant responses in the variation of the morphologies of tissues relative to those of the negative control. Nonetheless, uncoated GNPs demonstrated enhanced hepatotoxic outcomes relative to those of PEG-coated GNPs. The results demonstrated that both GNPs may be able to promote hepatotoxicity in Sprague Dawley rats through mechanisms of oxidative stress. However, uncoated GNPs have more harmful effects than PEG-coated GNPs relative to the negative control. CONCLUSION: Taken together, the results of this study indicate that PEG-coated GNPs may be safer to use in nanomedicinal applications than uncoated GNPs. However, more studies must be performed to confirm the outcomes of PEGylation.

State of the science review of the health effects of inorganic arsenic: Perspectives for future research.

Human exposure to inorganic arsenic (iAs) is a global health issue. Although there is strong evidence for iAs-induced toxicity at higher levels of exposure, many epidemiological studies evaluating its effects at low exposure levels have reported mixed results. We comprehensively reviewed the literature and evaluated the scientific knowledge on human exposure to arsenic, mechanisms of action, systemic and carcinogenic effects, risk characterization, and regulatory guidelines. We identified areas where additional research is needed. These priority areas include: (1) further development of animal models of iAs carcinogenicity to identify molecular events involved in iAs carcinogenicity; (2) characterization of underlying mechanisms of iAs toxicity; (3) assessment of gender-specific susceptibilities and other factors that modulate arsenic metabolism; (4) sufficiently powered epidemiological studies to ascertain relationship between iAs exposure and reproductive/developmental effects; (5) evaluation of genetic/epigenetic determinants of iAs effects in children; and (6) epidemiological studies of people chronically exposed to low iAs concentrations.

Low doses of multi-walled carbon nanotubes elicit hepatotoxicity in rats with markers of oxidative stress and induction of pro-inflammatory cytokines.

The investigation into the potential health risks associated with the use of engineered nanoparticles is a major scientific interest in recent years. The present study elucidated the involvement of pro-inflammatory cytokines, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in carboxylated multi-walled carbon nanotubes (MWCNTs)-induced hepatotoxicity. Pubertal rats were exposed to purified MWCNTs at 0, 0.25, 0.50, 0.75 and 1.0 mg/kg for 5 consecutive days. Results indicated that exposure to MWCNTs caused liver damage evidenced by significant elevation in serum activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and gamma glutamyl transferase (GGT) when compared with control. Moreover, MWCNTs significantly decreased superoxide dismutase (SOD) and glutathione S-transferase (GST) activities as well as glutathione level whereas it significantly increased catalase (CAT) and glutathione peroxidase (GPx) activities in liver of the treated rats. Moreover, the dose-dependent increase in hepatic hydrogen peroxide (H2O2) and lipid peroxidation levels were accompanied by marked increase in micronucleated polychromatic erythrocytes (MNPCE) in the MWCNTs-treated rats. Administration of MWCNTs significantly increased serum concentrations of pro-inflammatory cytokines namely interleukin-1ß (IL-1ß), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in the treated rats. Immunohistochemical analysis showed significantly increased COX-2 and iNOS protein expressions in the liver of MWCNTs-treated rats. In conclusion, carboxylated MWCNTs induces hepatic damage via disruption of antioxidant defense systems, promotion of pro-inflammatory cytokines generation and expression of COX-2 and i-NOS in rats.

Biochemical and histopathological evaluation of Al2O3 nanomaterials in kidney of Wistar rats.

The present study was conducted to evaluate the response of kidneys in Wistar rats following long-term exposure to Al2O3 nanomaterials (NMs). To achieve this objective, Al2O3 of three different sizes (30 nm, 40 nm and bulk) was orally administered for 28 days to 9 groups of 10 Wistar rats each at the dose of 500, 1000 and 2000 mg/kg/rat. A tenth group of 10 rats received distilled water and served as control. After 28 days of exposure the animals were sacrificed and the serum was collected and tested for the activity levels of creatinine and urea following standard methods. Induction of oxidative stress was also investigated by assessing thiobarbituric acid reactive substances (TBARS) (MDA), protein carbonyl, reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) activities. A histopathological evaluation was also performed to determine the extent of kidney damage. The results showed that both serum creatinine and serum urea levels increased significantly in the treated rats compared to control animals. The increase was found to be more in Al2O3-30 nm treated rats followed by Al2O3-40 nm and Al2O3-bulk treated rats in a dose-dependent manner. Further administration of Al2O3 significantly increased the activities of TBARS, protein carbonyl, catalase and decreased the activities of GSH and SOD in a dose-dependent manner in the kidney of rats compared with the control group. Histopathological evaluation showed significant morphological alterations in kidney tissues of treated rats in accordance with biochemical parameters. Taken together, the results of this study demonstrate that Al2O3 is nephrotoxic and its toxicity may be mediated through oxidative stress. Further, the results suggest that prolonged oral exposure to Al2O3 NMs has the potential to cause biochemical and histological alterations in kidney of rats at high concentration.

Toxicity Evaluation of Graphene Oxide in Kidneys of Sprague-Dawley Rats.

Recently, graphene and graphene-related materials have attracted a great deal of attention due their unique physical, chemical, and biocompatibility properties and to their applications in biotechnology and medicine. However, the reports on the potential toxicity of graphene oxide (GO) in biological systems are very few. The present study investigated the response of kidneys in male Sprague-Dawley rats following exposure to 0, 10, 20 and 40 mg/Kg GO for five days. The results showed that administration of GOs significantly increased the activities of superoxide dismutase, catalase and glutathione peroxidase in a dose-dependent manner in the kidneys compared with control group. Serum creatinine and blood urea nitrogen levels were also significantly increased in rats intoxicated with GO compared with the control group. There was a significant elevation in the levels of hydrogen peroxide and lipid hydro peroxide in GOs-treated rats compared to control animals. Histopathological evaluation showed significant morphological alterations of kidneys in GO-treated rats compared to controls. Taken together, the results of this study demonstrate that GO is nephrotoxic and its toxicity may be mediated through oxidative stress. In the present work, however, we only provided preliminary information on toxicity of GO in rats; further experimental verification and mechanistic elucidation are required before GO widely used for biomedical applications.

Responses of testis, epididymis, and sperm of pubertal rats exposed to functionalized multiwalled carbon nanotubes.

The present study investigated the response of testes, epididymides and sperm in pubertal Wistar rats following exposure to 0, 0.25, 0.5, 0.75, and 1.0 mg kg(-1) functionalized multi-walled carbon nanotubes (f-MWCNTs) for 5 days. The results showed that administration of (f-MWCNTs) significantly increased the activities of superoxide dismutase, catalase, and glutathione peroxidase in a dose-dependent manner in both testes and sperm compared with control group. Moreover, the significant decrease in the activity of glutathione-S-transferase and glutathione level was accompanied with significant elevation in the levels of hydrogen peroxide and malondialdehyde in both testes and sperm of (f-MWCNTs)-treated rats. The spermiogram of (f-MWCNTs)-treated rats indicated significant decrease in epididymal sperm number, sperm progressive motility, testicular sperm number and daily sperm production with elevated sperm abnormalities when compared with the control. Exposure to (f-MWCNTs) decreased plasma testosterone level and produced marked morphological changes including decreased geminal epithelium, edema, congestion, reduced spermatogenic cells and focal areas of tubular degeneration in the testes. The lumen of the epididymides contained reduced sperm cells and there was mild to severe hyperplasia epithelial cells lining the duct of the epididymis. Collectively, pubertal exposure of male rats to (f-MWCNTs) elicited oxidative stress response resulting in marked testicular and epididymides dysfunction.

Cytogenetic evaluation of functionalized single-walled carbon nanotube in mice bone marrow cells.

With their unique structure and physicochemical properties, single\-walled carbon nanotubes (SWCNTs) have many potential new applications in medicine and industry. However, there is lack of detailed information concerning their impact on human health and the environment. The aim of this study was to assess the effects, after intraperitoneal injection of functionalized SWCNTs (f-SWCNT) on the induction of reactive oxygen species (ROS), frequency of structural chromosomal aberrations (SCA), frequency of micronuclei induction, mitotic index, and DNA damage in Swiss-Webster mice. Three doses of f-SWCNTs (0.25, 0.5, and 0.75 mg/kg) and two controls (negative and positive) were administered to mice, once a day for 5 days. Bone marrow and peripheral blood samples were collected 24 h after the last treatment following standard protocols. F-SWCNT exposure significantly enhanced ROS, increased (p < 0.05) the number of SCA and the frequency of micronucleated cells, increased DNA damage, and decreased the mitotic index in exposed groups compared to negative control. The scientific findings reported here suggest that purified f-SWCNT have the potential to induce oxidative stress mediated genotoxicity in Swiss-Webster mice at higher level of exposure. Further characterization of their systemic toxicity, genotoxicity, and carcinogenicity is also essential. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1091-1102, 2016.

Hepatotoxicity and Ultra Structural Changes in Wistar Rats treated with Al2O3 Nanomaterials.

The present study was designed to evaluate the hepatotoxicity of aluminium oxide (Al2O3). To achieve this objective, Al2O3 of three different sizes (30nm, 40nm and bulk) was orally administered for 28 days to 9 groups of 10 Wistar rats each, at the dose of 500, 1000 and 2000 mg/Kg/rat. A tenth group of 10 rats received distilled water and served as control. After 28 days of exposure, the animals were sacrificed and the serum was collected and tested for the activity levels of aminotransferases (AST or GOT and ALT or GPT), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) enzymes following standard testing methods. Reduced glutathione (GSH) content was also measured in the liver tissue to study the oxidative stress. A histopathological evaluation was also performed to determine the extent of liver injury. Study results indicated that the activity of both the aminotransferases (AST and ALT), ALP and LDH increased significantly in Al2O3 treated rats compared to control animals. The increase was found to be more pronounced with Al2O3 - 30nm followed by Al2O3 - 40nm and Al2O3 - bulk treated rats in a dose dependent manner. However reduced glutathione content showed a decline in the activity. Ultra structural assessment showed significant morphological changes in the liver tissue in accordance with biochemical parameters. Taken together, the results of this study demonstrated that Al2O3 is hepatotoxic and the smaller size of this nanomaterial appeared to be the most toxic while the compound in the bulk form seemed to be the least toxic.

Genotoxicity study of silver nanoparticles in bone marrow cells of Sprague-Dawley rats.

The antimicrobial properties of silver nanoparticles (Ag-NPs) have resulted in their extensive application in consumer and health care products. Although Ag-NPs have great potential benefits, their side effects are unknown and seem inevitable due to their ability to reach the nucleus and damage genetic material. This study aimed to determine genotoxic potential of Ag-NPs using mitotic index (MI), DNA damage (comet assay), structural chromosome aberrations (SCA), micronuclei (MN) formation as genetic endpoints and induction of reactive oxygen species (ROS) as oxidative stress endpoint in bone marrow of Sprague-Dawley rats. Four groups of five male rats were orally administered Ag-NPs, once a day for five days with doses of 5, 25, 50, 100, mg/Kg. A control group was also made of five rats. Bone marrow samples were collected 24 h after the last treatment following standard protocols. Ag-NPs exposure significantly increased (p < 0.05) the induction of ROS, number of SCA, the frequency of micro-nucleated cells, damaged the DNA and decreased the mitotic index compared to negative control. The results suggest that Ag-NPs may have the potential to induce oxidative stress mediated genotoxicity in rats. Further characterization of their genotoxicity and also their potential health implications should be monitored regularly.

Silver nanoparticle-induced oxidative stress-dependent toxicity in Sprague-Dawley rats.

Due to the intensive commercial application of silver nanoparticles (Ag-NPs), their health risk assessment is of great importance. For acute toxicity evaluation of orally administered Ag-NPs, induction of reactive oxygen species (ROS), activity of liver function enzymes [(alanine (ALT/GPT), aspartate (AST/GOT), alkaline phosphatase (ALP)], concentration of lipid hydroperoxide (LHP), comet assay, and histopathology of liver in the rat model were performed. Four groups of five male rats were orally administered Ag-NPs, once a day for five days with doses of 5, 25, 50, 100 mg/kg, body weight. A control group was also made of five rats. Blood and liver were collected 24 h after the last treatment following standard protocols. Ag-NPs exposure increased the induction of ROS, activities of the liver enzymes (ALT, AST, ALP), concentration of lipid hydroperoxide (LHP), tail migration, and morphological alterations of the liver tissue in exposed groups compared to control. The highest two doses, 50 and 100 mg/kg showed statistically significant (p < 0.05) increases in ROS induction, ALT, AST, ALP activity, LHP concentration, DNA damage, and morphological alterations of liver compared to control. Based on these results, it is suggested that short-term administration of high doses of Ag-NP may cause organ toxicity and oxidative stress.

Arsenic-induced biochemical and genotoxic effects and distribution in tissues of Sprague-Dawley rats.

Arsenic (As) is a well documented human carcinogen. However, its mechanisms of toxic action and carcinogenic potential in animals have not been conclusive. In this research, we investigated the biochemical and genotoxic effects of As and studied its distribution in selected tissues of Sprague-Dawley rats. Four groups of six male rats, each weighing approximately 60 ± 2 g, were injected intraperitoneally, once a day for 5 days with doses of 5, 10, 15, 20 mg/kg bw of arsenic trioxide. A control group was also made of 6 animals injected with distilled water. Following anaesthetization, blood was collected and enzyme analysis was performed by spectrophotometry following standard protocols. At the end of experimentation, the animals were sacrificed, and the lung, liver, brain and kidney were collected 24 h after the fifth day treatment. Chromosome and micronuclei preparation was obtained from bone marrow cells. Arsenic exposure significantly increased (p<0.05) the activities of plasma alanine aminotransferase-glutamate pyruvate transaminase (ALT/GPT), and aspartate aminotransferase-glutamate oxaloacetate transaminase (AST/GOT), as well as the number of structural chromosomal aberrations (SCA) and frequency of micronuclei (MN) in the bone marrow cells. In contrast, the mitotic index in these cells was significantly reduced (p<0.05). These findings indicate that aminotransferases are candidate biomarkers for arsenic-induced hepatotoxicity. Our results also demonstrate that As has a strong genotoxic potential, as measured by the bone marrow SCA and MN tests in Sprague-Dawley rats. Total arsenic concentrations in tissues were measured by inductively coupled plasma mass spectrometry (ICP-MS). A dynamic reaction cell (DRC) with hydrogen gas was used to eliminate the ArCl interference at mass 75, in the measurement of total As. Total As doses in tissues tended to correlate with specific exposure levels.

Heavy metal toxicity and the environment.

Heavy metals are naturally occurring elements that have a high atomic weight and a density at least five times greater than that of water. Their multiple industrial, domestic, agricultural, medical, and technological applications have led to their wide distribution in the environment, raising concerns over their potential effects on human health and the environment. Their toxicity depends on several factors including the dose, route of exposure, and chemical species, as well as the age, gender, genetics, and nutritional status of exposed individuals. Because of their high degree of toxicity, arsenic, cadmium, chromium, lead, and mercury rank among the priority metals that are of public health significance. These metallic elements are considered systemic toxicants that are known to induce multiple organ damage, even at lower levels of exposure. They are also classified as human carcinogens (known or probable) according to the US Environmental Protection Agency and the International Agency for Research on Cancer. This review provides an analysis of their environmental occurrence, production and use, potential for human exposure, and molecular mechanisms of toxicity, genotoxicity, and carcinogenicity.

Genotoxicity of silver nanoparticles in Vicia faba: a pilot study on the environmental monitoring of nanoparticles.

The use of silver nanoparticles (AgNPs) in commercial products has increased significantly in recent years. Although there have been some attempts to determine the toxic effects of AgNPs in mammalian and human cell-lines, there is little information on plants which play a vital role in ecosystems. The study reports the use of Vicia faba root-tip meristem to investigate the genotoxicity of AgNPs under modified GENE-TOX test conditions. The root tip cells of V. faba were treated with four different concentrations of engineered AgNPs dispersion to study toxicological endpoints such as mitotic index (MI), chromosomal aberrations (CA) and micronucleus induction (MN). For each concentration, five sets of microscopy observations were carried out. The results demonstrated that AgNPs exposure significantly increased (p < 0.05) the number of chromosomal aberrations, micronuclei, and decreased the MI in exposed groups compared to control. From this study we infer that AgNPs might have penetrated the plant system and may have impaired mitosis causing CA and MN. The results of this study demonstrate that AgNPs are genotoxic to plant cells. Since plant assays have been integrated as a genotoxicity component in risk assessment for detection of environmental mutagens, they should be given full consideration when evaluating the overall toxicological impact of the nanoparticles in the environment.

Cytogenetic evaluation of malathion-induced toxicity in Sprague-Dawley rats.

Malathion is a well known pesticide and is commonly used in many agricultural and non-agricultural settings. Its toxicity has been attributed primarily to the accumulation of acetylcholine (Ach) at nerve junctions, due to the inhibition of acetylcholinesterase (AChE), and consequently overstimulation of the nicotinic and muscarinic receptors. However, the genotoxicity of malathion has not been adequately studied; published studies suggest a weak interaction with the genetic material. In the present study, we investigated the genotoxic potential of malathion in bone marrow cells and peripheral blood obtained from Sprague-Dawley rats using chromosomal aberrations (CAs), mitotic index (MI), and DNA damage as toxicological endpoints. Four groups of four male rats, each weighing approximately 60 ± 2g, were injected intraperitoneally (i.p.) once a day for five days with doses of 2.5, 5, 10, and 20mg/kg body weight (BW) of malathion dissolved in 1% DMSO. The control group was made up of four animals injected with 1% DMSO. All the animals were sacrificed 24h after the fifth day treatment. Chromosome preparations were obtained from bone marrow cells following standard protocols. DNA damage in peripheral blood leukocytes was determined using alkaline single-cell gel electrophoresis (comet assay). Malathion exposure significantly increased the number of structural chromosomal aberrations (CAs) and the percentages of DNA damage, and decreased the mitotic index (MI) in treated groups when compared with the control group. Our results demonstrate that malathion has a clastogenic/genotoxic potential as measured by the bone marrow CA and comet assay in Sprague-Dawley rats.