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Reports concerning the ineffectiveness of warfarin rodenticide, used at farms and stores in a rural area about 8 kilometers in diameter near Raleigh, North Carolina, prompted subsequent laboratory testing. All of the 25 Norway rats trapped from the area survived 6 days of no-choice feeding of bait containing 0.025 percent (by weight) warfarin.
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The rodenticide ANTU (alpha-naphthylthiourea) was used in the United Kingdom mainly in the late 1940s and early 1950s. The product then contained up to 0.2% of beta-naphthylamine as an impurity, and it was finally withdrawn in 1967 as a suspected carcinogen. Fourteen cases of urothelial tumours among rodent operatives exposed to ANTU are reported: in one district four out of 27 staff were affected, and in another area two out of 10. These cases strongly suggest that the early ANTU manufactured in the United Kingdom posed a cancer hazard to users. ANTU is still made or used in various countries, though the current product may be relatively pure and no longer contaminated by beta-naphthylamine. Recent laboratory evidence shows that even pure ANTU is mutagenic in the Ames test, and the safety of this rodenticide may need review.
The purpose of this study was to compare the excitability and contractility of three-dimensional skeletal muscle constructs, termed myooids, engineered from C2C12 myoblast and 10T1/2 fibroblast cell lines, primary muscle cultures from adult C3H mice, and neonatal and adult Sprague-Dawley rats. Myooids were 12 mm long, with diameters of 0.1-1 mm, were excitable by transverse electrical stimulation, and contracted to produce force. After approximately 30 days in culture, myooid cross-sectional area, rheobase, chronaxie, resting baseline force, twitch force, time to peak tension, one-half relaxation time, and peak isometric force were measured. Specific force was calculated by dividing peak isometric force by cross-sectional area. The specific force generated by the myooids was 2-8% of that generated by skeletal muscles of control adult rodents. Myooids engineered from C2C12-10T1/2 cells exhibited greater rheobase, time to peak tension, and one-half relaxation time than myooids engineered from adult rodent cultures, and myooids from C2C12-10T1/2 and neonatal rat cells had greater resting baseline forces than myooids from adult rodent cultures.
The total creatine (TCr) pool of skeletal muscle is composed of creatine (Cr) and phosphocreatine (PCr). In resting skeletal muscle, the ratio of PCr to TCr (PCr/TCr; PCr energy charge) is approximately 0.6-0.8, depending on the fiber type. PCr/TCr is linked to the cellular free energy of ATP hydrolysis by the Cr kinase equilibrium. Dietary Cr supplementation increases TCr in skeletal muscle. However, many previous studies have reported data indicating that PCr/TCr falls after supplementation, which would suggest that Cr supplementation alters the resting energetic state of myocytes. This study investigated the effect of Cr supplementation on the energy phosphates of resting skeletal muscle. Male rats were fed either rodent chow (control) or chow supplemented with 2% (wt/wt) Cr. After 2 wk on the diet, the gastrocnemius and soleus muscles were freeze clamped and removed from anesthetized animals. Cr supplementation increased TCr, PCr, and Cr levels in the gastrocnemius by 20, 22, and 17%, respectively (P < 0.05). A numerical 6% higher mean soleus TCr in Cr-supplemented rats was not statistically significant. All other energy phosphate concentrations, free energy of ATP hydrolysis, and PCr/TCr were not different between the two groups in either muscle. We conclude that Cr supplementation simply increased TCr in fast-twitch rat skeletal muscle but did not otherwise alter resting cellular energetic state.
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The total and specific indices of fleas, lice and mites were determined for ectoparasites on Rattus norvegicus norvegicus capture in urban areas of Belo Horizonte, Minas state, Brazil, from June 1980 to September 1982. In view of the limiting or critical values attributed to flea indices above all the "cheopis" index, proposed by several authors as a complementary measure for bubonic plague surveillance, the community of Belo Horizonte would have been exposed to this infection. The annual total indices ranged from 0.3 to 2.4 and the prevalent flea was Xenopsylla cheopis (99.2%), with the highest indices coinciding with the late dry-cool season. On two occasions, in this period, the community would have remained highly exposed to infection, since the index-limits were superseded: 8.8 (October 1980) and 6.2 (September 1982). It is suggested that preventive measures, such as protection against rat insecticide treatment may be efficiently applied in the late dry-cool season, or previous to the rainy season, before the elimination of rats. Reports on indices of lice and mites are important as they may establish index-limits for certain infections exclusive to rodents.
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Obesity and type II diabetes are closely related metabolic diseases with an increasing incidence worldwide. No clear-cut pharmacological treatment for these complex metabolic disturbances is available despite current efforts. New directions and perspectives for the pharmacological or nutritional treatment of these diseases should be defined. In recent years, a growing body of evidence shows that retinoids and retinoic acid receptors are involved in the control of biological aspects (e.g. adiposity and energy expenditure mechanisms), which offers great potential for research on the treatment of obesity and type II diabetes. All-trans retinoic acid is known to inhibit adipocyte differentiation, whereas, molecules activating the retinoid X-receptor (rexinoids) promote the differentiation of adipocytes. Treatment with rexinoids ameliorates glycemic control in rodent models of type II diabetes and obesity, although other findings indicate similar positive effects by inhibiting the receptor. Moreover, natural products of dietary origin, such as phytanic acid can activate RXR and thus, trigger adipose cell differentiation. Finally, the activation of retinoic acid receptors or retinoid X receptors has been reported to induce the gene expression of uncoupling proteins, which are mitochondrial proteins involved in the regulation of energy expenditure and fatty acid metabolism. Further research is required to exploit the capacities of the retinoid-dependent pathways of regulation of adiposity, insulin sensitivity and energy expenditure for drug development in metabolic disturbances.
The transcription factor networks that regulate basal and xenobiotic-modulated expression of the hepatic sulfotransferases affect the dynamics of xenobiotic detoxication, carcinogen bioactivation and metabolic homeostasis. Emerging evidence suggests that liver-enriched transcription factors, the aryl hydrocarbon (Ah) receptor and members of the nuclear receptor transcription factor superfamily all play integrated roles in the control of sulfotransferase gene transcription. Unlike the well known up-regulation of CYP1A1, expression of rat hepatic aryl (SULT1A1) and hydroxysteroid (SULT2A) sulfotransferase is suppressed in response to treatment with the prototypic Ah receptor ligand, 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin. Glucocorticoid-inducible rat hepatic SULT1A1 gene transcription occurs through a glucocorticoid receptor (GR)-mediated mechanism, while human hepatic SULT1A1 does not display GR-inducible expression. By comparison, liver-enriched transcription factors, such as CCAAT/enhancer binding protein, are essential for the maintenance of basal and GR-inducible rat hepatic SULT2A expression. The transcriptional control of rodent and human hepatic SULT2A expression is subject to trans-activation by the environmental sensor, pregnane X receptor (PXR). IR0 (inverted repeat with zero intervening bases) motifs located in the 5'-flanking regions of rodent SULT2A genes are required for transcriptional activation by PXR and other nuclear receptors, including constitutive androstane receptor, farnesoid X receptor and vitamin D receptor. Peroxisome proliferator activated receptor alpha (PPARalpha) mediates the induction of human, but not rat, hepatic SULT2A gene transcription, thus implicating a role for fatty acids as endogenous regulators of hepatic sulfonation in humans. This review focuses on the xenobiotic sensors and transcription factor systems that regulate sulfotransferase gene expression.
The success of gene therapy strongly depends on an efficient delivery system to allow local transfer and expression of the therapeutic gene in the target organ or tissue. Vector systems have been improved and many show promise. There are two different categories of delivery vehicles: non-viral and viral vectors, both with advantages and disadvantages that must be taken into consideration in view of the final aim. Compared to other solid organs, the kidney offers the main advantage of access by different routes that dictate different sites of transfection. Thus, the choice of the delivery vehicle and administration route has to take account which cells are to be specifically targeted by the gene transfer approach. This concept will be discussed in the first part of the review. Using a gene therapy approach, improvements of renal function and interstitial inflammation have been achieved in experimental models of glomerulonephritis and tubulo-interstitial damage. Gene therapy applied to renal transplantation has shown promising results in rodents, almost controlling acute rejection. Finally, the development of animal models resembling the clinical features of human genetic renal disorders offers a first step towards new treatments among which gene therapy could become reality in the near future. The main findings concerning the suitability of gene therapy for slowing the progression of kidney diseases, and preventing acute renal graft rejection, or treating genetic disorders, are discussed.
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