Oxidative stress has been implicated to play a role, at least in part, in pathogenesis of many disease conditions and toxicities in animals. Overproduction of reactive oxygen species and free radicals beyond the cells intrinsic capacity to neutralize following xenobiotics exposure leads to a state of oxidative stress and resultant damages of lipids, protein, and DNA. Lead and cadmium are the common environmental heavy metal pollutants and have widespread distribution. Both natural and anthropogenic sources including mining, smelting, and other industrial processes are responsible for human and animal exposure. These pollutants, many a times, are copollutants leading to concurrent exposure to living beings and resultant synergistic deleterious health effects. Several mechanisms have been explained for the damaging effects on the body system. Of late, oxidative stress has been implicated in the pathogenesis of the lead- and cadmium-induced pathotoxicity. Several ameliorative measures to counteract the oxidative damage to the body system aftermath or during exposure to these toxicants have been assessed with the use of antioxidants. The present review focuses on mechanism of lead- and cadmium-induced oxidate damages and the ameliorative measures to counteract the oxidative damage and pathotoxicity with the use of supplemented antioxidants for their beneficial effects.

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Oxidative Stress in Lead and Cadmium Toxicity and Its Amelioration

Alteration of testicular steroidogenesis and histopathology of reproductive system in male rats treated with triclosan.

Abstract In the past decades, much attention has been paid to toxicity assessment of nanoparticles prior to clinical and biological applications. While in vitro studies have been increasing constantly, in vivo studies of nanoparticles have not established a unified system until now. Predictive models and validated standard methods are imperative. This review summarizes the current progress in approaches assessing nanotoxicity in main systems, including the hepatic and renal, gastrointestinal, pulmonary, cardiovascular, nervous, and immune systems. Histopathological studies and specific functional examinations in each system are elucidated. Related injury mechanisms are also discussed.

https://www.degruyter.com/downloadpdf/j/ntrev.2017.6.issue-3/ntrev-2016-0047/ntrev-2016-0047.xml

Toxicity assessment of nanoparticles in various systems and organs

Although it is well known that cadmium (Cd) causes adverse effects on male rat reproductive organs, few studies have quantified alterations caused by its low doses. Quantification of these alterations, especially in the testis, was measured using morphometry. A single dose of cadmium chloride (1 or 1.2 mg/kg BW) was injected i.p. in adult rats, killed after 7 or 56 days. The lower dose caused slight alterations as measured by morphometrical analysis. The higher dose caused significant reduction in testis and epididymis weight, gonadossomatic index and length of seminiferous tubule (ST) after 7 and 56 days. Cadmium significantly reduced the ST diameter after 56 days. Decreased volume density of ST, after 7 and 56 days, was accompanied by an increase in interstitium volume density. The damage caused by the dose of 1.2 mg/kg can be clearly observed with light microscope. After 7 days, the tubule lumens were filled with degenerated germ cells and multinucleated spermatid aggregates. Vacuolization of the seminiferous epithelium was also observed. After 56 days, increased damage resulted in vacuolated ST, consisting only of Sertoli cells. Scanning electron microscopy examination of the testis showed that, in the group cadmium treated (1.2 mg/kg) and killed after 56 days, the interstitial tissue presents a compact and fibrous appearance with absence of fenestrae. The seminiferous epithelium height diminished and the absence of spermatozoa can be noted. The results show that a very small difference of Cd dose causes a sudden increase in testicular damage, apparently overpowering this tissue's natural defences.

Testis response to low doses of cadmium in Wistar rats.

There is a widespread repeated exposure of the population to the pesticides and heavy metals of occupational and environmental origin. Such population is forced to undergo continuous stress imposed by combined exposure of the heavy metals and different classes of the pesticides used in agricultural as well as health practices. The existing reports from several workers have indicated that heavy metals and pesticides in combination may lead more severe impact on the human health when compared to their individual effects. Such a combination of pesticides and heavy metals may also change or influence the detection of exposure. Several studies in past have shown the synergistic toxic effects of heavy metals and pesticides. Such evaluations have revealed the synergistic interactions of various heavy metals and pesticides in animals as well as humans. The aim of the present article is to provide a synthesis of existing knowledge on the synergistic effects of heavy metal and pesticides in living systems. The information included in this article may be useful for different environment protection agencies and policy makers to consider the combined effects of heavy metals and pesticides on humans while designing strategies towards environmental protection and safety regulations about human health.

/pdf/synergistic-effects-of-heavy-metals-and-pesticides-in-living-1r38bs0968.pdf

Synergistic Effects of Heavy Metals and Pesticides in Living Systems.

Effect of atenolol on cadmium-induced testicular toxicity in male rats

Background: Copper is essential as a trace element for metabolic processes. Exposure to copper in industries develops toxicity among the workers. Previous findings on adverse effects of copper on male reproductive function in adult albino rats led to investigate the effects of this metal on reproductive function of maturing male rats in the present experiment. Methodology: To study these effects, immature (30 to 35 days old) Wistar strain albino rats weighing about 50-60 g were treated intraperitoneally with copper chloride at doses of 1000, 2000 and 3000 µg/kg body weight/day for 26 days. Result: Significant fall in accessory sex organ weight and inhibition of testicular 17β-hydroxysteroid dehydrogenase activity along with degeneration of testicular growing spermatogenic cells and reduction in serum testosterone, FSH and LH level were observed at the doses of 2000 and 3000µg/kg/day. On the other hand, at the dose of 1000 µg/kg/day significant increase in testicular steroidogenic enzyme activity and stimulation of testicular spermatogenesis along with rise in serum testosterone and LH level were observed, though no significant change was observed in serum FSH level. This suggests that copper has got a dose-dependent effect on testicular steroidogenesis and spermatogenesis and serum testosterone and LH level in maturing male rats.

Dose-dependent effect of copper chloride on male reproductive function in immature rats

Copper chloride treatment adversely affects testicular activity in albino rats. To investigate its antitesticular effects mature (120 days) Wistar strain albino rats were treated intraperitoneally (i.p.) with copper chloride at doses of 1000, 2000 and 3000 μg/kg body weight/day for 26 days. Significant reduction of testicular and accessory sex organs (seminal vesicle, ventral prostate) weight, along with inhibition of testicular Δ5-3β-hydroxysteroid dehydrogenase (Δ5-3β-HSD) and 17β-hydroxysteroid dehydrogenase (17β-HSD) activity and reduction in plasma testosterone level, were observed at the doses of 2000 and 3000 μg/kg body weight/day. The degree of inhibition in all the parameters were increased with the increase of dosage. But no significant change was observed in the above parameters when the animals were treated with 1000 μg/kg body weight/day dose. This suggests that copper produces a suppressive influence on male reproductive activity, mainly on testicular weight and steroidogenesis and accessory sex organ weight in a dose-dependent manner.

Antitesticular effect of copper chloride in albino rats.

Effects of gold on testicular steroidogenic and gametogenic functions in immature male albino rats

Significant increase in ovarian and uterine weight and stimulation of ovarian delta5-3beta-hydroxysteroid dehydrogenase (delta5-3beta-HSD) activity and elevation of serum estradiol level were observed following gold chloride (0.2 mg/kg body weight/day), s.c. administration in immature female albino rats. Moreover, normal cyclic changes of estrus were found in vaginal smears of these rats whereas the rats of other groups showed diestrus phase throughout the period of experiment. Histological study of ovary also showed Graafian follicle with ovum in rats treated with 0.2 mg/kg/day of gold proving stimulation of reproductive function, which was not found in the ovarian histological study of other groups including controls. Thus, the results suggest a significant stimulatory effect of gold chloride on female reproductive activity in immature rats. Further, since the above-mentioned changes were evident at a specific dose of gold chloride, the data may have some clinical implications on stimulation and enhancement of fertility in immature female rats.

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A. Chattopadhyay

Papers

Effect of atenolol on cadmium-induced testicular toxicity in male rats

Dose-dependent effect of copper chloride on male reproductive function in immature rats

Antitesticular effect of copper chloride in albino rats.

Effects of gold on testicular steroidogenic and gametogenic functions in immature male albino rats

Effect of gold on stimulation of reproductive function in immature female albino rats.