Arsenate causes differential acute toxicity to two P-deprived genotypes of rice seedlings (Oryza sativa L.)

Significant genotypic difference in response to arsenate toxicity in rice (Oryza sativa) was investigated in root elongation, arsenate uptake kinetics, physiological and biochemical response and arsenic (As) speciation. Uptake kinetics data showed that P-deprived genotype 94D-54 had a little higher As uptake than P-deprived 94D-64, but the difference was not large enough to cause acute toxicity in P-deprived 94D-54. There was no difference in tissue P concentrations between the two genotypes under P deficient conditions. In addition, arsenic speciation in plant tissues (using high performance liquid chromatography-inductively coupled plasma mass spectrometry) was not different between P pretreatments and between genotypes. P-deprived genotype 94D-54 suffered much higher stress induced by arsenate toxicity than P-deprived genotype 94D-64, in terms of lipid peroxidation, tissue H2O2 concentrations and exosmosis of K, P and As. However, P-deprived 94D-54 also had higher overproduction of enzymatic antioxidants (with higher GPX, SOD, CAT) and NPT (non-protein thiols) than P-deprived 94D-64. It appeared that, the higher sensitivity of P-deprived 94D-54 to arsenate toxicity might cause the overproduction of NPT, thus leading to the depletion of GSH and to the accumulation of H2O2. The differential sensitivity of the two genotypes has major implications for breeding rice for As affected paddy soil.

Hip protectors to prevent hip fractures - a waste of time and money?

Abstract:
Background: An estimated 30-60% of older
adults fall every year and about 1% of falls result in a hip fracture. Hip fracture is a serious and growing problem, with a 3-10 fold rise in worldwide incidence predicted by 2050 (Gullberg, et al 1997). Hip protectors are underwear with built in protection for the greater trochanter. They are designed to prevent hip fractures by dispersing or absorbing the force of a fall. Trials
published to 2001 were broadly supportive of
the effectiveness of hip protectors, and this
was reflected in a Cochrane review in 2000.
However, earlier trials were methodologically
flawed and subsequent trials have not demonstrated effectiveness. The most recent Cochrane review describes only a marginal benefit (Parker et al, 2005).
Review and Discussion: This presentation
evaluates the current evidence for the use
of hip protectors and discusses the use of
that evidence by manufacturers, suppliers,
professional groups and guideline developers.
Interestingly, despite the limitations of the
evidence base, most advice has been broadly
supportive. Reasons for this are proposed
and discussed in the context of a critique of
evidence-based healthcare. protectors. However, the available evidence can be used in different ways and for different purposes by those with an interest in promoting
the use of hip protectors. A conservative
approach is warranted, where, if we cannot
demonstrate that hip protectors work, we
presume that they do not. This presentation will be of use to practitioners wanting to evaluate the evidence base for hip protectors (and other recommended interventions) on behalf of clients. It will also be of interest to policy makers who must assess the claims made for health care technologies as part of the decisionmaking process.
Recommended reading:
Gullberg B, Johnell O, Kanis JA (1997) Worldwide
projections for hip fracture. Osteoporos
Int. 7(5):407-13 .
Parker MJ, Gillespie WJ, Gillespie LD (2005) Hip
protectors for preventing hip fractures in older
people. The Cochrane Database of Systematic
Reviews Issue 3. Art. No.: CD001255.pub3. DOI:
10.1002/14651858.CD001255.pub3.

Nanoscale reinforced orthopaedic bone cement with graphene oxide - a possible solution to aseptic loosening of cemented hip implants? Preliminary results of an ongoing study

Hip replacement surgery is amongst the most common orthopaedic operations performed in the UK. Aseptic loosening is responsible for 40% of hip revision procedures. Aseptic loosening is a result of cement mantle fatigue. The aim of the current study is to analyse the effect of nanoscale Graphene Oxide (GO) on the mechanical properties of orthopaedic bone cement. Study Design A experimental thermal and mechanical analysis was conducted in a laboratory set up conforming to international standards for bone cement testing according to ISO 5583. Testing was performed on control cement samples of Colacryl bone cement, and additional samples reinforced with variable wt% of Graphene Oxide containing composites – 0.1%, 0.25%, 0.5% and 1.0% GO loading. Pilot Data Porosity demonstrated a linear relationship with increasing wt% loading compared to control (p<0.001). Thermal characterisation demonstrated maximal temperature during polymerization, and generated exotherm were inversely proportional to w%t loading (p<0.05) Fatigue strength performed on the control and 0.1 and 0.25%wt loadings of GO demonstrate increased average cycles to failure compared to control specimens. A right shift of the Weibull curve was demonstrated for both wt% available currently. Logistic regression analysis for failure demonstrated significant increases in number of cycles to failure for both specimens compared to a control (p<0.001). Forward Plan Early results convey positive benefits at low wt% loadings of GO containing bone cement. Study completion and further analysis is required in order to elude to the optimum w%t of GO which conveys the greatest mechanical advantage.

Is differential phytochelatin production related to decreased arsenate influx in arsenate tolerant Holcus lanatus?

Phytochelatins (PCs) are required for arsenic (As) detoxification in nontolerant plants. In addition, a role for PCs in arsenate tolerance has recently been proven, with tolerant plants able to accumulate significantly higher concentrations of As-PC complexes at equivalent levels of stress than nontolerant plants. The relationship between arsenate influx and PC production in tolerant and non-tolerant Holcus lanatus plants was determined in this study, along with an investigation of the effect of inhibition of PC synthesis by buthionine sulfoximine (BSO) on arsenate tolerance. A strong correlation between PC production and arsenate influx was demonstrated in arsenate-tolerant plants. In addition, inhibition of PC synthesis by BSO in tolerant plants increased arsenate sensitivity to that of the nontolerant clone. This dramatic reduction in tolerance proves that PC production is an essential component of the arsenate tolerance mechanism in H. lanatus. This study proposes that while there is a single major gene for arsenate tolerance, hypostatic modifiers are also in operation, affecting the expression of the tolerance character. © New Phytologist (2002).

Differential susceptibility of mitochondrial complex II to inhibition by oxaloacetate in brain and heart

Mitochondrial Complex II is a key mitochondrial enzyme connecting the tricarboxylic acid (TCA) cycle and the electron transport chain. Studies of complex II are clinically important since new roles for this enzyme have recently emerged in cell signalling, cancer biology, immune response and neurodegeneration. Oxaloacetate (OAA) is an intermediate of the TCA cycle and at the same time is an inhibitor of complex II with high affinity (Kd ~ 10− 8 M). Whether or not OAA inhibition of complex II is a physiologically relevant process is a significant, but still controversial topic. We found that complex II from mouse heart and brain tissue has similar affinity to OAA and that only a fraction of the enzyme in isolated mitochondrial membranes (30.2 ± 6.0% and 56.4 ± 5.6% in the heart and brain, respectively) is in the free, active form. Since OAA could bind to complex II during isolation, we established a novel approach to deplete OAA in the homogenates at the early stages of isolation. In heart, this treatment significantly increased the fraction of free enzyme, indicating that OAA binds to complex II during isolation. In brain the OAA-depleting system did not significantly change the amount of free enzyme, indicating that a large fraction of complex II is already in the OAA-bound inactive form. Furthermore, short-term ischemia resulted in a dramatic decline of OAA in tissues, but it did not change the amount of free complex II. Our data show that in brain OAA is an endogenous effector of complex II, potentially capable of modulating the activity of the enzyme.