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 known that opioids regulate luteinizing hormone (LH) secretion through not fully understood mechanisms. This study describes the effects of naloxone on the episodic release of LH in adult sham-operated and pituitary-grafted female rats. Animals were rendered hyperprolactinemic by transplanting 2 pituitary glands beneath the kidney capsule. Naloxone (2 mg/kg/h) or saline (0.5 ml/h) were administered iv through jugular cannulae and subjects were bled at 7 min intervals for a period of 3 h. As expected, pituitary-grafting was followed by an increase in mean values of prolactin during the bleeding period. Naloxone administration decreased mean serum prolactin levels in sham-operated rats and did not further change them in pituitary-grafted animals. Hyperprolactinemia was associated with increases in mean serum LH levels during the bleeding period and in the absolute amplitude of LH peaks. Naloxone administration increased mean values of LH and the absolute amplitude of LH peaks, and decreased their frequency in sham-operated rats. Neither pituitary grafting nor naloxone administration modified the frequency, duration or relative amplitude of LH peaks. However, naloxone administration reduced the mean half-life of LH in sham-operated rats to a similar extent than did pituitary grafting. Naloxone failed to further change the mean half-life of LH in pituitary-grafted rats. These results suggest that opioids modulate the pulsatile pattern of LH and that these effects are blunted in pituitary-grafted animals.

Effects of naloxone on pulsatile luteinizing hormone in experimental hyperprolactinemia.

Acute versus subchronic expossure to cadmium differentially affects the pulsatile secretion pattern of prolactin in adult male rats

Are toxic effects of cadmium on the pulsatile prolactin secretion mediated by TRH

Regulation of prolactin secretion involves complex interactions of multiple inhibitory and stimulatory factors. Among them, luteinizing hormone-releasing hormone (LHRH) has been shown, when analyzed in single samples, to exert both stimulatory and inhibitory influences on prolactin secretion. In the present study, we have further examined the effects of LHRH on prolactin secretion by studying the pulsatile pattern of the hormone after the administration of the neuropeptide. For this purpose, adult sham-operated and pituitary-grafted female rats, exhibiting diestrus smears were bled for 3 hr during the morning (1030 to 1330 hr). Two pulses of LHRH (10 ng/kg body wt) were administered 60 and 120 min after starting the bleeding period. Pituitary grafting increased the mean serum prolactin levels, absolute amplitude of the hormone peaks, and its mean half-life, compared with control animals. In sham-operated rats, LHRH administration diminished mean serum prolactin levels, the absolute pulse amplitude and frequency of prolactin peaks. In pituitary-grafted animals, LHRH administration only decreased the pulse frequency of prolactin peaks. These data suggest that LHRH significantly suppressed pulsatile prolactin secretion, and that this effect was blunted by exposure to previously elevated circulating prolactin levels.

Anunciación Lafuente

Papers

Effects of naloxone on pulsatile luteinizing hormone in experimental hyperprolactinemia.

Acute versus subchronic expossure to cadmium differentially affects the pulsatile secretion pattern of prolactin in adult male rats

Are toxic effects of cadmium on the pulsatile prolactin secretion mediated by TRH

Effects of Luteinizing Hormone-Releasing Hormone on Pulsatile Prolactin Secretion in Adult Hyperprolactinemic Female Rats