Toxicity Of Nanoparticles Research Articles

Enhancement of Triple-Negative Breast Cancer-Specific Induction of Cell Death by Silver Nanoparticles by Combined Treatment with Proteotoxic Stress Response Inhibitors.

Metal nanoparticles have been tested for therapeutic and imaging applications in pre-clinical models of cancer, but fears of toxicity have limited their translation. An emerging concept in nanomedicine is to exploit the inherent drug-like properties of unmodified nanomaterials for cancer therapy. To be useful clinically, there must be a window between the toxicity of the nanomaterial to cancer and toxicity to normal cells. This necessitates identification of specific vulnerabilities in cancers that can be targeted using nanomaterials without inducing off-target toxicity. Previous studies point to proteotoxic stress as a driver of silver nanoparticle (AgNPs) toxicity. Two key cell stress responses involved in mitigating proteotoxicity are the heat shock response (HSR) and the integrated stress response (ISR). Here, we examine the role that these stress responses play in AgNP-induced cytotoxicity in triple-negative breast cancer (TNBC) and immortalized mammary epithelial cells. Furthermore, we investigate HSR and ISR inhibitors as potential drug partners to increase the anti-cancer efficacy of AgNPs without increasing off-target toxicity. We showed that AgNPs did not strongly induce the HSR at a transcriptional level, but instead decreased expression of heat shock proteins (HSPs) at the protein level, possibly due to degradation in AgNP-treated TNBC cells. We further showed that the HSR inhibitor, KRIBB11, synergized with AgNPs in TNBC cells, but also increased off-target toxicity in immortalized mammary epithelial cells. In contrast, we found that salubrinal, a drug that can sustain pro-death ISR signaling, enhanced AgNP-induced cell death in TNBC cells without increasing toxicity in immortalized mammary epithelial cells. Subsequent co-culture studies demonstrated that AgNPs in combination with salubrinal selectively eliminated TNBCs without affecting immortalized mammary epithelial cells grown in the same well. Our findings provide additional support for proteotoxic stress as a mechanism by which AgNPs selectively kill TNBCs and will help guide future efforts to identify drug partners that would be beneficial for use with AgNPs for cancer therapy.

In vitro safety profile and phyto-ecotoxicity assessment of the eco-friendly calcium oxide nanoparticles

The present study aims to evaluate the toxicity of the green calcium oxide nanoparticles (CaO-NPs) from golden linseed extract (Linum usitatissimum L.) by phytotoxicity in seeds (Daucus carota, Beet shankar, Lactuca sativa and Brassica oleracea), in vitro safety profile and soil toxicity for CaO-NPs solutions from 12.5 to 100 μg mL−1. Ecotoxicity analysis of the soil was conducted using XRD diffractograms, which revealed characteristic peaks of the nanoparticles at 37.35° (12.5, 25, 50, and 100 μg mL−1), as well as a peak at 67.34° (25 and 100 μg mL−1). Additionally, the in vitro safety assessment indicated favorable cell specification and regulation within the first 24 h, demonstrating reductions of 15.9 ± 0.2%, 17.9 ± 0.2%, 17.6 ± 0.2%, and 32.9 ± 0.2% to 12.5, 25, 50, and 100 μg mL−1, respectively. The dsDNA assay revealed initial protection and controlled release within the cells for 48 h. However, after 72 h, there was an increase of 20 ± 0.2%, 16 ± 0.2%, 32 ± 0.2%, and 43 ± 0.2% to 12.5, 25, and 50 μg mL−1. The analysis of ROS generation demonstrated a reduction of 40 ± 0.2%, 33 ± 0.2%, 20 ± 0.2%, and 9 ± 0.2% to 12.5, 25, 50, and 100 μg mL−1, respectively, within 72 h. When compared to the negative control (NC), there was an increase of 50 ± 0.2%, 56 ± 0.2%, 77 ± 0.2%, and 92 ± 0.2% at the same concentrations, suggesting that the nanoparticles generated free radicals, leading to cellular inflammation. This was attributed to the positive surface charge of the nanoparticles, resulting in reduced interaction with the cell membrane and the subsequent release of hydroxyl (•OH), which caused inflammatory processes in the cells. Therefore, CaO-NPs exhibited a low phytotoxicity and high cytocompatibility, while also promoting plant germination and growth.

Black sand nanoparticles and heat stress impacts the neurological and oxidative stress indices and splenic-renal histology of Clarias gariepinus

In Egypt, while many studies have focused on the radiometry and mineralogy of black sands, research on their effects on nearby aquatic organisms is rare. This study aimed to assess the combined effects of heat stress (HS) and black sand nanoparticles (BS-NPs) on renal function, antioxidant responses (TAC, SOD, CAT), neuro-stress indicators (AchE, cortisol), and to conduct histopathological investigations in the kidney and spleen tissues of African catfish Clarias gariepinus over a 15-day period to exposure to control, HS (32 °C), BS (6.4 g/kg diet) and HS + BS groups. The outcomes revealed that thermal stress alone showed no significant difference from the control. However, creatinine and uric acid levels were significantly higher in the BS-NPs and HS + BS-NPs groups (p < 0.001). Antioxidant markers (TAC, SOD, and CAT) were substantially reduced across all treated groups (0.05 ≥ p < 0.0001). AchE levels were significantly elevated in BS-NPs and HS + BS-NPs (p < 0.001), while cortisol levels were higher in these groups but not significantly different in HS. Degeneration and necrosis in the white and red pulps, scattered lymphocytes, and increased collagen fiber surrounding blood vessels and the lining of the ellipsoid structure were all evident in the spleen, along with the enlargement of the melanomacrophage centers with big granular, irregular, and brown pigments (hemosiderin). Our study, therefore, provides new insights into how heat stress, an abiotic environmental factor, influences the toxicity of black sand nanoparticles in catfish.

Hazardous effects of nickel ferrite nanoparticles and nickel chloride in early life stages of the freshwater snail Biomphalaria glabrata (Say, 1818).

Nickel ferrite nanoparticles (NiF NPs) have growing applications in biomedical and nanomedicine fields. However, knowledge concerning their ecotoxicity during the early developmental stages of invertebrates, such as gastropods, remains scarce. Thus, the current study aimed to evaluate whether NiF NPs and nickel chloride (NiCl2) induce toxic effects on embryos and newly hatched snails of freshwater species Biomphalaria glabrata (Say, 1818). NiF NPs were synthesized and characterized by multiple techniques, and their ecotoxicity was assessed by Biomphalaria embryotoxicity test (BET) during 144h of exposure and an acute toxicity test (96h) using newly hatched snails. NiF NPs induced mortality, developmental delay, reduced hatching rate, and promoted morphological changes in B. glabrata. Also, NiF NPs induced higher toxicity in embryos than in newly hatched B. glabrata. Overall, results showed that the early developmental stages of gastropods are a target group for nanoparticle toxicity in freshwater ecosystems.

Investigation of the biological activity and toxicity of bioactive silver nanoparticles synthesized via Vitex agnus-castus seed extract on honey bees

Investigation of the biological activity and toxicity of bioactive silver nanoparticles synthesized via Vitex agnus-castus seed extract on honey bees

Activated hedgehog and insulin ligands by decreased transcriptional factor DAF-16 mediate transgenerational nanoplastic toxicity in Caenorhabditis elegans

In Caenorhabditis elegans, transcriptional factor DAF-16 in insulin signaling pathway played important role in regulating transgenerational nanoplastic toxicity. Activation of insulin signals mediated transgenerational toxicity of polystyrene nanoparticle (PS-NP) by inhibiting DAF-16. Among identified germline ligands, expression of wrt-3 encoding hedgehog ligand was increased by RNAi of daf-16 in PS-NP exposed C. elegans. In PS-NP exposed C. elegans, expressions of 4 other germline hedgehog ligand genes and 10 hedgehog receptor genes were increased by daf-16 RNAi. Among these candidate genes, expressions of hedgehog ligand genes (grl-15, grl-16, qua-1, and wrt-1) and hedgehog receptor genes (ptr-23, scp-1, ptd-2, and ncr-1) could be increased by PS-NP (1–100 μg/L), and their transgenerational expressions were observed after PS-NP exposure. RNAi of grl-15, grl-16, qua-1, wrt-1, ptr-23, scp-1, ptd-2, and ncr-1 caused resistance to transgenerational PS-NP toxicity. In nematodes exposed to PS-NPs, RNAi of wrt-3, grl-15, grl-16, qua-1, and wrt-1 at parental generation (P0-G) inhibited expressions of ptr-23, scp-1, ptd-2, and ncr-1 in their offspring. Moreover, we observed increased expressions of insulin peptides genes (ins-3, ins-39, and daf-28) in PS-NP exposed daf-16(RNAi) nematodes, suggesting formation of feedback loop. We raise the molecular basis for formation of toxicity on multiple generations after nanoplastic exposure at P0-G.

Metallic and metallic oxide nanoparticles toxicity primarily targets the mitochondria of hepatocytes and renal cells.

Nanoparticles (NPs) are utilized in various applications, posing potential risks to human health, tissues, cells, and macromolecules. This study aimed to investigate the ultrastructural alterations in hepatocytes and renal tubular cells induced by metallic and metal oxide NPs. Adult healthy male Wistar albino rats (Rattus norvegicus) were divided into 6 (n = 7) control and 6 treated groups (n = 7). The rats in the treated groups exposed daily to silver NPs, gold NPs, zinc oxide NPs, silicon dioxide NPs, copper oxide NPs, and ferric oxide NPs for 35 days. The members of the control group for each corresponding NPs received the respective vehicle. Liver and kidney tissue blocks from all rats were processed for Transmission Electron Microscopy (TEM) examinations. The hepatocytes and renal tubular cells of all NPs-treated rats demonstrated mitochondrial ultrastructural alterations mainly cristolysis, swelling, membrane disruption, lucent matrices, matrices lysis, and electron-dense deposits. However, other organelles demonstrated injury but to a lesser extent in the form of shrunken nuclei, nuclear membrane indentation, endoplasmic reticulum fragmentation, cellular membranes enfolding, brush border microvilli disruption, lysosomal hyperplasia, ribosomes dropping, and peroxisome formation. One may conclude from the findings that the hepatocytes and the renal tubular cells mitochondria are the main targets for nanoparticles toxicity ending in mitochondrial disruption and cell injury. Further studies taking into account the relation of mitochondrial ultrastructural damage with a weakened antioxidant defense system induced by chronic exposure to nanomaterials are needed.

In silico Investigations of Al2O3 and NiO Nanoparticles Interactions with Antioxidant Enzymes of Fresh Water Fish O.mossambicus

Metal oxide nanoparticles caused hazardous to aquatic organisms, especially fishes. Nanomaterials of Aluminium and nickel oxide are applied in wide range of applications. However the toxicity of these metal oxide nanoparticles on freshwater fish is very scarce. In this study, we investigated the toxic impact of these two nanoparticles through an in silico approach. The antioxidant enzymes /proteins of SOD, CAT and GST in fish O.mossambicus were docked against Al2O3 and NiO NPs. These enzymes are responsible for oxidative metabolism of a large number of nanomaterials. Induction of oxidative stress by NPs exposure leads to inhibition of these enzymes. The targeted proteins SOD, CAT and GST were retrieved from Alpha fold database and docked with ligands. Molecular docking was conducted using CB - Dock and AutoDock Vina software tools to find the binding affinity and interaction with amino acids of each protein. The target proteins found to strongly interact with ligands through hydrogen bonding and metal coordination interactions. The lowest binding energy shows strong binding of ligands with proteins. Docking results revealed that the amino acids residues of SOD, CAT and GST enzymes are strongly bind with the Al2O3 and NiO NPs in its active site and causes inhibition of the enzymes activities. CAT exhibited lowest binding affinity of (-4.0 Kcal/mol) among all enzymes and significantly inhibited by NiO NPs, followed by GST (-3.4 Kcal/mol), likewise CAT (-1.7 Kcal/mol) and GST (-1.8 Kcal/mol) was moderately inhibited by Al2O3 NPs. SOD inhibited insignificantly by both the NPs. In conclusion, NiO NPs effectively inhibit antioxidant enzymes activity than Al2O3 NPs.

Assessing the toxicity of green Agaricus bisporus-based Cadmium Sulfide nanoparticles on Musca domestica as a biological model

The common housefly, Musca domestica, known for transmitting over 100 infections, was studied using green-synthesized Cadmium Sulfide nanoparticles (CdS NPs) from Agaricus bisporus. These CdS NPs were tested on third-instar larvae under laboratory conditions using dipping and feeding methods with concentrations (75, 100, 125, 150, 175, and 200 µg/mL). The toxicity, measured by LC50, was found to be 138 µg/mL for dipping treatment and 123 µg/mL for feeding treatment. Analysis with an energy-dispersive X-ray microanalyzer confirmed Cd accumulation in the larval midgut, indicating penetration of CdS NPs into the organism, which may potentially increase their toxicity. CdS NPs caused disruptions in Heat Shock Protein 70, cell apoptosis, and various biochemical components. Scanning electron microscopy revealed morphological abnormalities in larvae, pupae, and adults exposed to CdS NPs. Ultrastructural examination showed significant midgut tissue abnormalities in larvae treated with 123 µg/mL of CdS NPs. Our study demonstrated that green-synthesized CdS NPs from A. bisporus can effectively control the development of M. domestica larvae.

Ellagic acid-enhanced biocompatibility and bioactivity in multilayer core-shell gold nanoparticles for ameliorating myocardial infarction injury

BackgroundMyocardial infarction (MI) is the main contributor to most cardiovascular diseases (CVDs), and the available post-treatment clinical therapeutic options are limited. The development of nanoscale drug delivery systems carrying natural small molecules provides biotherapies that could potentially offer new treatments for reactive oxygen species (ROS)-induced damage in MI. Considering the stability and reduced toxicity of gold-phenolic core-shell nanoparticles, this study aims to develop ellagic acid-functionalized gold nanoparticles (EA-AuNPs) to overcome these limitations.ResultsWe have successfully synthesized EA-AuNPs with enhanced biocompatibility and bioactivity. These core-shell gold nanoparticles exhibit excellent ROS-scavenging activity and high dispersion. The results from a label-free imaging method on optically transparent zebrafish larvae models and micro-CT imaging in mice indicated that EA-AuNPs enable a favorable excretion-based metabolism without overburdening other organs. EA-AuNPs were subsequently applied in cellular oxidative stress models and MI mouse models. We found that they effectively inhibit the expression of apoptosis-related proteins and the elevation of cardiac enzyme activities, thereby ameliorating oxidative stress injuries in MI mice. Further investigations of oxylipin profiles indicated that EA-AuNPs might alleviate myocardial injury by inhibiting ROS-induced oxylipin level alterations, restoring the perturbed anti-inflammatory oxylipins.ConclusionsThese findings collectively emphasized the protective role of EA-AuNPs in myocardial injury, which contributes to the development of innovative gold-phenolic nanoparticles and further advances their potential medical applications.Graphical

Sustainable Biofuel Production Utilizing Nanotechnology: Challenges and Potential Solutions

ABSTRACTThe transition to biofuels as viable alternatives to fossil fuels is increasingly critical, given the rising demand for sustainable energy. However, biofuel production is hindered by challenges such as feedstock scarcity, elevated production costs, and environmental impacts. Nanotechnology has the potential to significantly improve the efficiency and durability of biofuel production processes, thereby overcoming these challenges. Although there has been significant research on using nanomaterials in biofuel production, there needs to be more emphasis on understanding and addressing the difficulties of integrating these materials and developing strategies to overcome them. This review systematically examines the role of nanotechnology in various biofuel production pathways, including biodiesel, biogas, bioethanol, biohydrogen, hydrotreated vegetable oils, and Fischer–Tropsch synthesis. We discuss how nanomaterials improve key aspects of biofuel production, such as catalysis, microbial conversion, biomass pretreatment, and separation. Despite these advancements, nanotechnology has challenges, including nanoparticle toxicity, increased operational costs, and technical limitations. We propose potential solutions to these issues, emphasizing the need for interdisciplinary collaboration and innovative approaches. By effectively integrating nanotechnology into biofuel production, the energy sector can move toward a more sustainable and environmentally friendly future.

Stereological and biochemical effects of thymoquinone on ovarian tissue toxicity induced by silver nanoparticles in NMRI mice: An experimental study.

The toxicity of silver nanoparticles (AgNPs) has been proven in the female reproductive system. Thymoquinone (TQ) is a natural antioxidant and bioactive component of Nigella sativa. We evaluated the efficacy of TQ on ovarian tissue following toxicity induced by AgNPs in female mice. 24 female NMRI mice (5-6 wk, an average weight of 33 gr) were randomly divided into 4 groups (n = 6/each): control, AgNPs (500 mg/kg, gavage), TQ (2.5 mg/kg, intraperitoneal injection), and TQ+AgNPs. Mice were treated every day for 35 days. Serum levels of malondialdehyde (MDA), total antioxidant capacity (TAC), luteinizing hormone, and follicle-stimulating hormone were measured. The optical disector and stereological techniques were utilized to estimate the follicular count, their volume at different developmental stages, and the structure of ovarian tissue. In the AgNPs group, the serum concentrations of TAC (p = 0.01), luteinizing hormone (p 0.001), follicle-stimulating hormone, the volume of corpus luteum (p 0.001), and the number of follicles decreased significantly compared to the control group. Nevertheless, AgNPs significantly increased the MDA level. In the TQ+AgNPs group compared to the AgNPs group, a significant decrease in MDA level (p 0.001) and a significant improvement in TAC (p = 0.03), and hormonal levels, the number of primary, preantral, and antral follicles (p = 0.04), and the volume of corpus luteum (p = 0.01) were observed. TQ improved the number of follicles by reducing oxidative stress and lipid peroxidation in AgNPs-damaged ovarian tissue.

Dynamics of Phytotoxicity Indicators of Ordinary Chernozem when it is Contaminated with Silver Nanoparticles

The dynamics of phytotoxicity indicators (germination and length of radish roots) of ordinary chernozem when contaminated with silver nanoparticles was studied. In laboratory conditions, ordinary chernozem was contaminated with silver nanoparticles (1, 10 and 100 mg/kg) for 3, 10, 30, 90 and 180 days. It was found that the more silver nanoparticles were introduced into the soil, the greater the decrease in germination and length of radish roots. There was no restoration of germination and length of radish roots with an increase in the period from the moment of contamination. In this study, the maximum toxic period from the moment of contamination for each indicator was identified by its sensitivity to silver nanoparticles and informativeness. The maximum toxicity of silver nanoparticles in relation to the root length and germination of radishes was noted on the 10th and 30th days, respectively. The results can be used to assess the phytotoxicity of soils contaminated with silver nanoparticles.

Single and combined effects of titanium (TiO2) and zinc (ZnO) oxide nanoparticles in the rainbow trout gill cell line RTgill-W1.

Understanding the environmental impact of nanoparticle (NP) mixtures is essential to accurately assess the risk they represent for aquatic ecosystems. However, although the toxicity of individual NPs has been extensively studied, information regarding the toxicity of combined NPs is still comparatively rather scarce. Hence, this research aimed to investigate the individual and combined toxicity mechanisms of two widely consumed nanoparticles, zinc oxide (ZnO NPs) and titanium dioxide (TiO2 NPs), using an in vitro model, the RTgill-W1 rainbow trout gill epithelial cell line. Sublethal concentrations of ZnO NPs (0.1µgmL-1) and TiO2 (30µgmL-1) and a lethal concentration of ZnO NPs causing 10% mortality (EC10, 3µgmL-1) were selected based on cytotoxicity assays. Cells were then exposed to the NPs at the selected concentrations alone and to their combination. Cytotoxicity assays, oxidative stress markers, and targeted gene expression analyses were employed to assess the NP cellular toxicity mechanisms and their effects on the gill cells. The cytotoxicity of the mixture was identical to the one of ZnO NPs alone. Enzymatic and gene expression (nrf2, gpx, sod) analyses suggest that none of the tested conditions induced a strong redox imbalance. Metal detoxification mechanisms (mtb) and zinc transportation (znt1) were affected only in cells exposed to ZnO NPs, while tight junction proteins (zo1 and cldn1), and apoptosis protein p53 were overexpressed only in cells exposed to the mixture. Osmoregulation (Na + /K + ATPase gene expression) was not affected by the tested conditions. The overall results suggest that the toxic effects of ZnO and TiO2 NPs in the mixture were significantly enhanced and could result in the disruption of the gill epithelium integrity. This study provides new insights into the combined effects of commonly used nanoparticles, emphasizing the importance of further investigating how their toxicity may be influenced in mixtures.

P21-48 Toxicity of subway related nanoparticles in human lung cell models

P21-48 Toxicity of subway related nanoparticles in human lung cell models

Photoperiod-dependent effects of zinc oxide nanoparticles on the growth and reproduction of Daphnia pulex

The discharge of metal nanoparticles into the water inevitably poses a threat to aquatic organisms and the balance of the aquatic ecosystem. Photoperiod is one of the most important ecological factors for the development of cladocerans. In addition, different light conditions can also affect the toxicity of metal nanoparticles. In this study, we studied the effects of four photoperiods (8L/16D, 10L/14D, 14L/10D, and 16L/8D) combined with three concentrations of ZnO NPs (0 mg L−1, 0.05 mg L−1, and 0.10 mg L−1) on the growth and reproduction of Daphnia pulex. With the increase of photoperiod, the maternal body size and growth rate increased first and then decreased; the first time to reproduction was advanced, and broods and the total offspring also increased. Under the influence of ZnO NPs, growth rate and reproductive capacity were inhibited. The photoperiod 8L/16D and 16L/8D interacted with ZnO NPs on the growth of D. pulex, which significantly decreased the growth rate. Besides, the interaction between photoperiod 8L/16D and ZnO NPs decreased the reproduction ability of D. pulex. These results suggest that the effects of zinc oxide nanoparticles on the growth and reproduction of D. pulex is photoperiod dependent, which is useful for assessing the risk of pollutants to cladoceras under different light conditions.

P21-63 Towards an understanding of the relative toxicity of nanoparticles from different transport sources

P21-63 Towards an understanding of the relative toxicity of nanoparticles from different transport sources

P04-02 Adverse outcome pathways to support assessment of food nanoparticles toxicity on gut microbiota and intestinal barrier integrity

P04-02 Adverse outcome pathways to support assessment of food nanoparticles toxicity on gut microbiota and intestinal barrier integrity

Transgenerational response of germline histone acetyltransferases and deacetylases to nanoplastics at predicted environmental doses in Caenorhabditis elegans

Nanoplastics could cause toxic effects on organism and their offsprings; however, how this transgenerational toxicity is formed remains largely unclear. We here examined potential involvement of germline histone acetylation regulation in modulating transgenerational toxicity of polyetyrene nanoparticle (PS-NP) in Caenorhabditis elegans. At parental generation (P0-G), PS-NP (1–100 μg/L) decreased expressions of germline cbp-1 and taf-1 encoding histone acetyltransferases, as well as germline expressions of sir-2.1 and hda-3 encoding histone deacetylase. Decrease in these 4 germline genes were also observed in the offspring of PS-NP (1–100 μg/L) exposed nematodes. Germline RNAi of cbp-1, taf-1, sir-2.1 and hda-3 resulted in more severe transgenerational PS-NP toxicity on locomotion and brood size. Meanwhile, in PS-NP exposed nematodes, germline RNAi of cbp-1, taf-1, sir-2.1 and hda-3 increased expression of genes encoding insulin, FGF, Wnt, and/or Notch ligands and expressions of their receptor genes in the offspring. Susceptibility to transgenerational PS-NP toxicity in cbp-1(RNAi), taf-1(RNAi), sir-2.1(RNAi), and hda-3 (RNAi) was inhibited by RNAi of these germline ligands genes. Moreover, histone deacetylase inhibition served as molecular initiating event (MIE) leading to transgenerational toxicity in epigenetic adverse outcome pathway (AOP) for nanoplastics. Our data provided evidence that germline histone acetylation regulation functioned as an important mechanism for transgenerational toxicity of nanoplastics at predicted environmental doses (PEDs) by affecting secreted ligands in organisms.

Effects of changed water regime on the toxicity of silver nanoparticles (AgNPs) in tadpoles of Fejervarya limnocharis.

Climate change is viewed as one of the important causes of the amphibian population decline. Aspects of climate change like increase in water temperature and drying up of habitats have been underrepresented. The expanding production and usage of metal nanoparticles like silver nanoparticles (AgNPs) make them likely to end up in aquatic ecosystems. To arrive at a realistic assessment of the impact of AgNPs in a warming world, we have investigated the effects of temperature on the acute toxicity of AgNPs in tadpoles of Fejervarya limnocharis at 24, 48, 72 and 96h of exposure. The various aspects of sub-lethal toxicities of AgNPs with increase in temperature were also investigated. Besides, the effects of habitat desiccation on the sub-lethal toxicities of AgNPs in the tadpoles were analysed. The LC50 values of AgNPs at four different time points were found to be significantly different between the two different temperatures. Alterations in survival pattern, life history traits, amplifications in genotoxic potential and oxidative stress were observed with increased water temperature following AgNP exposure. The phenomenon of habitat desiccation was also found to significantly affect the toxicity of AgNPs with respect to alterations in mortality rate, time to metamorphosis and morphometric parameters of metamorphosed tadpoles. The findings suggest that changed water regime such as increased water temperature as well as reduction in water level accelerated the toxic effects of AgNPs in F. limnocharis tadpoles which is likely to affect their natural populations.