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Sex-dependent Differences (sex-dependent + difference)

Distribution by Scientific Domains

Life Sciences	50%

Selected Abstracts

Organochlorine pesticides and mercury in cottonmouths (Agkistrodon piscivorus) from northeastern Texas, USA,

ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 3 2005
Thomas R. Rainwater
Abstract Dspite their ecological importance andglobal decline, snakes remain poorly studied in ecotoxicology. In this study, we examined organochlorine (OC) pesticide and mercury accumulation in cottonmouths (Agkistrodon piscivorus) living on a contaminated site in northeastern Texas (USA). Mercury and p,p,-dichlorodiphenyldichloroethylene (p,p,-DDE) were detected in all snakes examined. Other OCs, including p,p,-dichlorodiphenyltrichloroethane (p,p,-DDT), methoxychlor, aldrin, and heptachlor, also were detected, but less frequently. Concentrations of p,p,-DDE were higher in fat than in liver, while mercury concentrations were highest in liver, followed by kidney and tail clips. One animal contained the highest mercury concentration yet reported for a snake (8,610 ng/g). Mercury concentrations in liver and kidney were higher in males than females, while no intersex differences in p,p,-DDE concentrations were observed. Concentrations of p,p,-DDE in fat were correlated positively with body size in male cottonmouths but not females, suggesting a slower rate of accumulation in females. Body size strongly predicted mercury concentrations in liver, kidney, and tail clips of both sexes. Tail clips were strong predictors of mercury in liver and kidney in males but not females, suggesting possible sex-dependent differences in mercury toxicokinetics. Both long-term field studies and controlled laboratory investigations are needed to adequately assess the response of cottonmouths to chronic contaminant exposure. [source]

Cardiac and coronary function in the Langendorff-perfused mouse heart model

EXPERIMENTAL PHYSIOLOGY, Issue 1 2009
Melissa E. Reichelt
The Langendorff mouse heart model is widely employed in studies of myocardial function and responses to injury (e.g. ischaemia). Nonetheless, marked variability exists in its preparation and functional properties. We examined the impact of early growth (8, 16, 20 and 24 weeks), sex, perfusion fluid [Ca2+] and pacing rate on contractile function and responses to 20 min ischaemia followed by 45 min reperfusion. We also assessed the impact of strain, and tested the utility of the model in studying coronary function. Under normoxic conditions, hearts from 8-week-old male C57BL/6 mice (2 mm free perfusate [Ca2+], 420 beats min,1) exhibited 145 ± 2 mmHg left ventricular developed pressure (LVDP). Force development declined by ,15% (126 ± 5 mmHg) with a reduction in free [Ca2+] to 1.35 mm, and by 25% (108 ± 3 mmHg) with increased pacing to 600 beats min,1. While elevated heart rate failed to modify ischaemic outcome, the lower [Ca2+] significantly improved contractile recovery (by >30%). We detected minimal sex-dependent differences in normoxic function between 8 and 24 weeks, although age modified contractile function in males (increased LVDP at 24 versus 8 weeks) but not females. Both male and female hearts exhibited age-related reductions in ischaemic tolerance, with a significant decline in recovery evident at 16 weeks in males and later, at 20,24 weeks, in females (versus recoveries in hearts at 8 weeks). Strain also modified tolerance to ischaemia, with similar responses in hearts from C57BL/6, 129/sv, Quackenbush Swiss and FVBN mice, but substantially greater tolerance in BALB/c hearts. In terms of vascular function, baseline coronary flow (20,25 ml min,1 g,1) was 50,60% of maximally dilated flows, and coronary reactive and functional hyperaemic responses were pronounced (up to 4-fold elevations in flow in hearts lacking ventricular balloons). These data indicate that attention to age (and sex) of mice will reduce variability in contractile function and ischaemic responses. Even small differences in perfusion fluid [Ca2+] also significantly modify tolerance to ischaemia (whereas modest shifts in heart rate do not impact). Ischaemic responses are additionally strain dependent, with BALB/c hearts displaying greatest intrinsic tolerance. Finally, the model is applicable to the study of vascular reactivity, providing large responses and excellent reproducibility. [source]

Estradiol inhibits chondrogenic differentiation of mesenchymal stem cells via nonclassic signaling

ARTHRITIS & RHEUMATISM, Issue 4 2010
Zsuzsa Jenei-Lanzl
Objective We undertook this study to examine the effects of estradiol on chondrogenesis of human bone marrow,derived mesenchymal stem cells (MSCs), with consideration of sex-dependent differences in cartilage repair. Methods Bone marrow was obtained from the iliac crest of young men. Density-gradient centrifugation,separated human MSCs proliferated as a monolayer in serum-containing medium. After confluence was achieved, aggregates were created and cultured in a serum-free differentiation medium. We added different concentrations of 17,-estradiol (E2) with or without the specific estrogen receptor inhibitor ICI 182.780, membrane-impermeable E2,bovine serum albumin (E2-BSA), ICI 182.780 alone, G-1 (an agonist of G protein,coupled receptor 30 [GPR-30]), and G15 (a GPR-30 antagonist). After 21 days, the aggregates were analyzed histologically and immunohistochemically; we quantified synthesized type II collagen, DNA content, sulfated glycosaminoglycan (sGAG) concentrations, and type X collagen and matrix metalloproteinase 13 (MMP-13) expression. Results The existence of intracellular and membrane-associated E2 receptors was shown at various stages of chondrogenesis. Smaller aggregates and significantly lower type II collagen and sGAG content were detected after treatment with E2 and E2-BSA in a dose-dependent manner. Furthermore, E2 enhanced type X collagen and MMP-13 expression. Compared with estradiol alone, the coincubation of ICI 182.780 with estradiol enhanced suppression of chondrogenesis. Treatment with specific GPR-30 agonists alone (G-1 and ICI 182.780) resulted in a considerable inhibition of chondrogenesis. In addition, we found an enhancement of hypertrophy by G-1. Furthermore, the specific GPR-30 antagonist G15 reversed the GPR-30,mediated inhibition of chondrogenesis and up-regulation of hypertrophic gene expression. Conclusion The experiments revealed a suppression of chondrogenesis by estradiol via membrane receptors (GPR-30). The study opens new perspectives for influencing chondrogenesis on the basis of classic and nonclassic estradiol signaling. [source]

The Biochemistry of Drug Metabolism , An Introduction

CHEMISTRY & BIODIVERSITY, Issue 12 2008
Part 6.
Abstract This review is part of a series of review articles on the metabolism of drugs and other xenobiotics published in Chemistry & Biodiversity. After a thorough discussion of metabolic reactions and their enzymes, this article focuses on genetically determined differences in drug and xenobiotic metabolism. After a short introduction on the causes for genetic differences, the first focus is on species differences in drug and xenobiotic metabolism. A major chapter is then dedicated to clinically relevant genetic polymorphisms in human drug metabolism and resultant ethnic differences. The last two chapters deal with sex-dependent differences in drug metabolism and personalized pharmacotherapy related to inter-individual differences in drug metabolism. [source]