Microbial degradation of petroleum hydrocarbons.

Today nanotechnology is finding growing applications in industry, biology, and medicine. The clear benefits of using nanosized products in various biological and medical applications are often challenged by concerns about the lack of adequate data regarding their toxicity. One area of interest involves the interactions between nanoparticles and the components of the immune system. Nanoparticles can be engineered to either avoid immune system recognition or specifically inhibit or enhance the immune responses. We review herein reported observations on nanoparticle-mediated immunostimulation and immunosuppression, focusing on possible theories regarding how manipulation of particle physicochemical properties can influence their interaction with immune cells to attain desirable immunomodulation and avoid undesirable immunotoxicity.

Minireview: Nanoparticles and the Immune System

Effects of currently used pesticides in assays for estrogenicity, androgenicity, and aromatase activity in vitro.

Cadmium (Cd2+) is a common environmental pollutant and a major constituent of tobacco smoke. Exposure to this heavy metal, which has no known beneficial physiological role, has been linked to a wide range of detrimental effects on mammalian reproduction. Intriguingly, depending on the identity of the steroidogenic tissue involved and the dosage used, it has been reported to either enhance or inhibit the biosynthesis of progesterone, a hormone that is inexorably linked to both normal ovarian cyclicity and the maintenance of pregnancy. Thus, Cd2+ has been shown to exert significant effects on ovarian and reproductive tract morphology, with extremely low dosages reported to stimulate ovarian luteal progesterone biosynthesis and high dosages inhibiting it. In addition, Cd2+ exposure during human pregnancy has been linked to decreased birth weights and premature birth, with the enhanced levels of placental Cd2+ resulting from maternal exposure to industrial wastes or tobacco smoke being associated with decreas...

Endocrine disruption by cadmium, a common environmental toxicant with paradoxical effects on reproduction.

Cadmium (Cd) is a heavy metal that has received considerable concern environmentally and occupationally. Cd has a long biological half-life mainly due to its low rate of excretion from the body. Thus, prolonged exposure to Cd will cause toxic effect due to its accumulation over time in a variety of tissues, including kidneys, liver, central nervous system (CNS), and peripheral neuronal systems. Cd can be uptaken from the nasal mucosa or olfactory pathways into the peripheral and central neurons; for the latter, Cd can increase the blood brain barrier (BBB) permeability. However, mechanisms underlying Cd neurotoxicity remain not completely understood. Effect of Cd neurotransmitter, oxidative damage, interaction with other metals such as cobalt and zinc, estrogen-like, effect and epigenetic modification may all be the underlying mechanisms. Here, we review the in vitro and in vivo evidence of neurotoxic effects of Cd. The available finding indicates the neurotoxic effects of Cd that was associated with both biochemical changes of the cell and functional changes of central nervous system, suggesting that neurotoxic effects may play a role in the systemic toxic effects of the exposure to Cd, particularly the long-term exposure.

https://downloads.hindawi.com/journals/omcl/2013/898034.pdf

Cadmium and Its Neurotoxic Effects

It is well established that cadmium affects plasma levels of the pituitary hormones studied. However, whether the effects of the metal are dose dependent needs to be clarify. This work was designed to evaluate the possible changes in plasma levels of gonadotropins, prolactin, ACTH, GH and TSH after oral cadmium exposure in adult male rats. Plasma levels of these hormones were measured in adult male rats exposed to cadmium chloride (CdCl2) in the drinking water at the doses of 5, 10, 25, 50 or 100 ppm for one month. The lower dose of cadmium increased plasma prolactin levels and higher doses of the metal (25 or 50 ppm) decreased them. There was a continuous increase of plasma ACTH levels from the lower to 25 ppm dose of CdCl2 and decreased them after to basal values with the highest dose. Plasma GH levels were increased with the dose of cadmium of 10 ppm, although the doses of 5, 25 and 50 ppm decreased them. Plasma LH levels were only reduced with the dose of 50 ppm of CdCl2, whereas those of FSH increased. Plasma TSH levels were increased with the doses of 5, 25 and 100 ppm of CdCl2. Cadmium concentration increased in pituitary with the doses of 125, 50 and 100 ppm of CdCl2. These data suggest that cadmium differentially affects the secretory mechanisms of the pituitary hormones studied depending on the dose used. The effects of the metal on prolactin and ACTH are dose-dependent.

Are cadmium effects on plasma gonadotropins, prolactin, ACTH, GH and TSH levels, dose-dependent?

The hypothalamic–pituitary–gonadal axis is target of cadmium toxicity. An update of recent studies and potential therapeutic approaches

This study analyzes cadmium effects at the hypothalamic-pituitary-testicular axis. Male rats were given cadmium during puberty or adulthood. Cadmium exposure through puberty increased norepinephrine content in all hypothalamic areas studied, but not in the median eminence. Metal exposure increased serotonin turnover in median eminence and the anterior hypothalamus, while decreased it in mediobasal hypothalamus. Also, decreased plasma levels of testosterone were found. Cadmium exposure during adulthood increased norepinephrine content in posterior hypothalamus and decreased the neuro-transmitter content in anterior and mediobasal hypothalamus. Decreased circulating levels of luteinizing hormone (LH) and testosterone and increased plasma follicle stimulating hormone (FSH) levels were also observed. Cadmium accumulated in all analyzed tissues. Various parameters showed age-dependent changes. These data suggest that cadmium globally effects hypothalamic-pituitary-testicular axis function by acting at the three levels analyzed and that an interaction between cadmium exposure and age emerge.

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Papers

Are cadmium effects on plasma gonadotropins, prolactin, ACTH, GH and TSH levels, dose-dependent?

The hypothalamic–pituitary–gonadal axis is target of cadmium toxicity. An update of recent studies and potential therapeutic approaches

Cadmium effects on hypothalamic-pituitary-testicular axis in male rats.

Pubertal and postpubertal cadmium exposure differentially affects the hypothalamic-pituitary-testicular axis function in the rat.

Initial study on the effects of Prestige oil on human health.