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Increased application of engineered nanoparticles in different sectors viz. agriculture, commerce, industry, and medicine has raised serious public health issues. Nanoparticles of nickel have been increasingly used as catalysts, conductive pastes, adhesives, nanowires, and nanofilters. Human and animal exposure to these particles may cause toxicity in different organs/systems. Studies made in the past had demonstrated their toxicity in liver, kidney, and lungs. However, their reproductive effects remain poorly understood. Therefore, the present study on reproductive toxicity of nickel nanoparticles (<30 nm) was executed in female Wistar rats. A comparison of results obtained in nickel microparticle-treated rats was also made. Rats were administered nano and microparticles through gavage at a dosage of 5 mg/kg body weight each for two exposure periods; that is, 15 and 30 days. Ovaries removed from these rats were analyzed to study the effects of nickel bioaccumulation on synthesis of steroid hormones, lipid peroxidation, apoptosis, and oxidative stress. Structural changes were monitored through histopathological and ultrastructural observations. The present study showed exposure time-dependent differences in the toxicity of nickel nano and microparticles in the ovary of rats. Nano nickel was cumulative in the ovaries. It affected steroidogenesis. Further, increased generation of reactive oxygen species and enhanced oxidative stress may have contributed to cytotoxicity. It was concluded that exposure to nano nickel might induce irreversible damage in the ovaries of rat.

Phthalate compounds are widely used industrial chemicals; when incorporated into polyvinyl chloride, they are not covalently bound and released into the surrounding media. Some of them have estrogenic potential in vitro but data on in vivo studies are scanty. For the 3-day uterotrophic assay, di-n-butyl phthalate (DBP;10 and 100 mg/kg), butyl benzyl phthalate (BBP; 20 and 200 mg/kg), and diethylstilbestrol (DES, 40 µg/kg, positive control) were administered orally to immature female rats for three consecutive days from postnatal day (PND) 21. For the 20-day pubertal onset assay, DBP (10 and 20 mg/kg), BBP (20 and 200 mg/kg), and DES (6 µg/kg) were administered orally from PND 21 daily for 20 days. In the uterotrophic assay, in groups treated with higher dose of DBP and BBP, the uterine wet weight significantly decreased in the higher dose, and there were minor variations in the ovary wet weight, while the wet weight of these organs increased significantly in DES-treated group. In the 20-day pubertal assay, the weight of uterus and ovary declined significantly and changes in vaginal weight were nonsignificant in DBP- and BBP-treated groups. However, in DES-treated group nonsignificant elevation in vagina weight was observed. All the DES-treated animals showed the vaginal opening (VO) on day 26.17 ± 0.16. However, VO was not observed in any of the animals in control, vehicle control, BBP-, and DBP-treated groups up to PND 42, except in one animal each in vehicle control and DBP (100 mg/kg)-treated groups. The data indicated that both DBP and BBP were unable to induce elevation in the uterine and ovarian weight. While DES treatment can accelerate the growth of uterus and ovary and alter the onset of puberty and estrous cyclicity in prepubertal rats. These suggest that these compounds may not have estrogenic potential in vivo., (© The Author(s) 2012.)

Some ingredients of panmasala have the ability to penetrate the blood-testis barrier but the reproductive toxic potential of panmasala has not been studied. This study is aimed to assess the possible damage caused by panmasala to male reproductive system in mice. Swiss albino male mice were randomly divided into 7 groups receiving either standard control diet or panmasala-containing diet. Three doses (0.5%, 1.5% and 3%) of panmasala plain (PMP) as well as panmasala with tobacco (PMT)-gutkha were given for a period of 6 months. Assessment of organ weight, sperm count and morphology, spermatid count, sperm production, testicular 17β-hydroxysteroid dehydrogenase (17β-HSD) activity and histology were conducted. A nonsignificant decrease in absolute and relative weight of testis and epididymis was observed. Spermatid count, sperm count and production were significantly decreased and 17β-HSD activity was found considerably declined at 3% of both PMP- and PMT-treated groups as compared to control. The histological observations revealed panmasala induced testicular damage. Abnormal morphology of sperm head shape was significantly elevated in higher doses of both types of panmasala-treated groups than control. The results suggests that panmasala has reproductive toxic potential and more alteration is seen with gutkha as compared to panmasala plain, indicating that similar effects might also be possible in humans.

Toxicity of dye containing effluent of tannery, textile, dyes and pulp-paper industries was evaluated in an acute toxicity test using Daphnia magna. The 48-hour EC(50) values were 4.33% and 19.5% for tannery effluents (Tn1 and Tn2). Textile effluents (Tx1-Tx7) had 48-hour EC(50) values; >100%, >100%, 62.9%, 63.0%, 40.3%, >100% and >100%, respectively. Dye industries (D1-D7) had 48-hour EC(50) values; 14.1%, 15.5%, 24.5%, 29.7%, 23.2%, >100% and >100%, respectively. Similarly pulp-paper effluents (P1-P5) showed acute toxicity as 100%, 77.87%, 46.44%, 69.55% and 82.84%, respectively. These results showed linear relationship with high degree of confidence (r(2) ≥ 0.84-0.99) between immobility and test concentrations. Toxicity classification criteria showed that out of five effluents from pulp-paper mill, four were minor acutely toxic having 48-hour EC(50) value in between >46%-100%. Out of seven textile effluents, four were not acutely toxic (48-hour EC(50) value >100%) and three were minor acutely toxic (48-hour EC( 50) value in the range of 40.3%-63.0%). Similarly, out of seven dye industrial effluents, two were not acutely toxic and five minor acutely toxic. One of the two tanneries was moderately acutely toxic and another one was minor acutely toxic. Classification based on toxic unit revealed that four out of five pulp-paper effluent, three out of seven textile effluents, five out of seven dye effluents and both the tannery effluents were toxic. Overall, 66.67% effluents were found toxic and 33.33% as non-toxic. In general, tannery and dyes effluents showed more toxicity than textile and paper mill effluents.

Pan masala is commonly consumed in south-east Asian and other oriental countries as an alternate of tobacco chewing and smoking. Genotoxic potential of pan masala (pan masala plain and pan masala with tobacco known as gutkha) was evaluated employing chromosome aberration (CA) and micronucleus (MN) assay in vivo. Animals were exposed to three different doses (0.5%, 1.5% and 3%) of pan masala plain (PMP) and gutkha (PMT) through feed for a period of 6 months and micronucleus and chromosomal aberrations were studied in the bone marrow cells. Induction of mean micronuclei in polychromatic erythrocytes (MNPCE) and normochromatic erythrocyte (MNNCE) was higher in both types of pan masala treated groups with respect to control group. Both pan masala plain and gutkha treatment significantly induced the frequency of MNPCE and MNNCE in the bone marrow cells, indicating the genotoxic potential. Furthermore, slight decline in the ratio of polychromatic erythrocytes to normochromatic erythrocytes was also noticed, suggesting the cytotoxic potential even though the ratio was statistically non significant. A dose-dependent, significant increase in chromosome aberration was observed in both types of pan masala treated mice with respect to control. However, no significant difference in micronucleus and chromosomal aberration induction was noticed between two types of pan masala exposed (PMP and PMT) groups. Results suggest that both types of pan masala, i.e. plain and gutkha, have genotoxic potential.

Aquatic toxicity of textile dyes and textile and dye industrial effluents were evaluated in an acute toxicity study using Daphnia magna as an aquatic experimental animal model. The 48-h EC(50) value for the azo dyes, Remazol Parrot Green was 55.32 mg/L and for Remazol Golden Yellow was 46.84 mg/L. Whereas 48-h EC(50) values for three dye industrial effluents (D1, D2, and D3) were 14.12%, 15.52%, and 29.69%, respectively. Similarly, EC(50) value for three textile mill effluents (T1, T2, and T3) were >100%, 62.97%, and 63.04%, respectively. These results also showed linear relationship with high degree of confidence (r(2)A =A >0.84 to >0.99) between immobility and test concentrations. The ratio of 24 to 48-h EC(50) remains to be in between 1.1 and 1.2. The general criteria of toxicity classification showed that both dyes were minor acutely toxic having 48-h EC(50) in between 10 and 100 mg/L. Of the six textile and dye industrial effluents tested, one was not acutely toxic (48-h EC(50)A >A 100%) and five were minor acutely toxic (48-h EC(50)A >A 14.12-29.69%). The toxicity classification of effluent based on toxic unit (TU) showed that of the six effluents tested five were found toxic (TU = >1) and one was non-toxic (TU = <1). Thus, dye effluents showed highest toxicity and textile effluents lowest toxicity. The study also suggested that the assay with D.A magna was an excellent method for evaluation of aquatic toxicity of dyes and dyes containing industrial effluents.