Evidence for the Cost of Reproduction in Humans: High Lifetime Reproductive Effort Is Associated with Greater Oxidative Stress in Post-Menopausal Women

Life history theory predicts trade-offs between reproductive effort and maternal survivorship in energy-restricted environments. However, empirical evidence for the positive association between maternal mortality and reproductive effort from energetically challenged human populations are mixed and physiological mechanisms that may underlie this association are poorly understood. We hypothesized that increases in aerobic metabolism during repeated periods of pregnancy and lactation result in increased oxidative stress that may contribute to somatic deterioration, vulnerability to illness, and accelerated aging. We therefore predicted that lifetime gravidity and parity would be related to levels of biomarkers of oxidative stress, as well as antioxidative defence enzymes in post-menopausal women. Our hypothesis was supported by positive linear associations between levels of 8-OHdG, a biomarker of DNA oxidative damage (β = 0.21, p<0.05), levels of antioxidative defence enzyme Cu-Zn SOD (β = 0.25, p<0.05), and number of lifetime pregnancies. Furthermore, independent of age and health status, post-menopausal women with higher gravidity and parity (> = 4 pregnancies per lifetime) had 20% higher levels of 8-OHdG and 60% higher levels of Cu-Zn SOD compared to women with lower gravidity and parity (<4 pregnancies per lifetime). Our results present the first evidence for oxidative stress as a possible cost of reproductive effort in humans.     

8-OHdG在医学领域的应用与研究进展

氧化应激带来的氧化损伤是造成人体多种损伤和病变的重要因素。8-羟基脱氧鸟苷(8-hydroxy-2’-deoxyguanosine,8-OHdG)作为DNA氧化损伤产物是广泛用于研究疾病中氧化损伤机制的关键标志物。国内外大量研究已普遍应用8-OHdG作为分析指标,该文着眼于近年来研究动向,就8-OHdG的作用机理与检测方法,以及职业与环境暴露的危害评价、辅助疾病早期诊断、治疗和新药研发等方面的应用作一综述。     

Chloroacetonitrile (CAN) induces glutathione depletion and 8-hydroxylation of guanine bases in rat gastric mucosa

Chloroacetonitrile (CAN) is detected in drinking-water supplies as a by-product of the chlorination process. Gastroesophageal tissues are potential target sites of acute and chronic toxicity by haloacetonitriles (HAN). To examine the mechanism of CAN toxicity, we studied its effect on glutathione (GSH) homeostasis and its impact on oxidative DNA damage in gastric mucosal cells of rats. Following a single oral dose (38 or 76 mg/Kg) of CAN, animals were sacrificed at various times (0-24 h), and mucosa from pyloric stomach were collected. The effects of CAN treatment on gastric GSH contents and the integrity of genomic gastric DNA were assessed. Oxidative damage to gastric DNA was evaluated by measuring the levels of 8-Hydroxydeoxyguanosine (8-OHdG) in hydrolyzed DNA by HPLC-EC. The results indicate that CAN induced a significant, dose- and time-dependent, decrease in GSH levels in pyloric stomach mucosa at 2 and 4 hours after treatment (56 and 39% of control, respectively). DNA damage was observed electrophoretically at 6 and 12 hours following CAN administration. CAN (38 mg/Kg) induced significant elevation in levels of 8-OHdG in gastric DNA. Maximum levels of 8-OHdG in gastric DNA were observed at 6 hours after CAN treatment [9.59+/-0.60 (8-OHdG/10(5)dG) 146% of control]. When a high dose of CAN (76 mg/Kg) was used, a peak level of 8-OHdG [11.59+/-1.30 (8-OHdG/10(5)dG) 177% of control] was observed at earlier times (2 h) following treatment. When CAN was incubated with gastric mucosal cells, a concentration-dependent cyanide liberation and significant decrease in cellular ATP levels were detected. These data indicate that a mechanism for CAN-induced toxicity may be partially mediated by depletion of glutathione, release of cyanide, interruption of the energy metabolism, and induction of oxidative stress that leads to oxidative damage to gastric DNA.     

Age‐specific oxidative status and the expression of pre‐ and postcopulatory sexually selected traits in male red junglefowl, Gallus gallus

Oxidative stress is emerging as a key factor underpinning life history and the expression of sexually selected traits. Resolving the role of oxidative stress in life history and sexual selection requires a pluralistic approach, which investigates how age affects the relationship between oxidative status (i.e., antioxidants and oxidative damage) and the multiple traits contributing to variation in reproductive success. Here, we investigate the relationship between oxidative status and the expression of multiple sexually selected traits in two‐age classes of male red junglefowl, Gallus gallus, a species which displays marked male reproductive senescence. We found that, irrespective of male age, both male social status and comb size were strongly associated with plasma oxidative status, and there was a nonsignificant tendency for sperm motility to be associated with seminal oxidative status. Importantly, however, patterns of plasma and seminal antioxidant levels differed markedly in young and old males. While seminal antioxidants increased with plasma antioxidants in young males, the level of seminal antioxidants remained low and was independent of plasma levels in old males. In addition, old males also accumulated more oxidative damage in their sperm DNA. These results suggest that antioxidant allocation across different reproductive traits and somatic maintenance might change drastically as males age, leading to age‐specific patterns of antioxidant investment.     

Oxidative damage and plasma antioxidant capacity in relation to body size,age, male sexual traits and female reproductive performance in the collared flycatcher (<Emphasis Type="Italic">Ficedula albicollis</Emphasis>)

The study of oxidative stress is a potential tool for studying the functional interactions among life history traits, sexual traits and physiological status in animals. In this study, we investigated relationships between measures of plasma oxidative status and male sexual traits, female reproductive investment and three other life history traits, in a wild population of collared flycatchers (Ficedula albicollis). Flycatcher males with a larger white forehead patch had higher level of plasma antioxidant capacity. For females, clutch size was not associated with plasma oxidative status, but egg size was positively correlated with antioxidant capacity. The relationship between age and levels of plasma oxidative damage remains controversial in this species: young female flycatchers showed higher levels of hydroperoxides compared to antioxidants, whereas age did not predict oxidative status of males. Males had higher levels of oxidative damage than females, although the concentration of antioxidant compounds was similar between the sexes. Females that mated with more ornamented males had higher plasma antioxidant capacity. Our results suggest that, for males and females, greater investment in sexual signal and reproduction, respectively, does not reduce the capacity for self-maintenance or avoidance of oxidative stress. Finally, our data support indirectly the occurrence of assortative mating in our species, since females with higher plasma antioxidant capacity mated with more ornamented males.     

Oxidative shielding and the cost of reproduction

Life‐history theory assumes that reproduction and lifespan are constrained by trade‐offs which prevent their simultaneous increase. Recently, there has been considerable interest in the possibility that this cost of reproduction is mediated by oxidative stress. However, empirical tests of this theory have yielded equivocal support. We carried out a meta‐analysis to examine associations between reproduction and oxidative damage across markers and tissues. We show that oxidative damage is positively associated with reproductive effort across females of various species. Yet paradoxically, categorical comparisons of breeders versus non‐breeders reveal that transition to the reproductive state is associated with a step‐change reduction in oxidative damage in certain tissues and markers. Developing offspring may be particularly sensitive to harm caused by oxidative damage in mothers. Therefore, such reductions could potentially function to shield reproducing mothers, gametes and developing offspring from oxidative insults that inevitably increase as a consequence of reproductive effort. According to this perspective, we hypothesise that the cost of reproduction is mediated by dual impacts of maternally‐derived oxidative damage on mothers and offspring, and that mothers may be selected to diminish such damage. Such oxidative shielding may explain why many existing studies have concluded that reproduction has little or no oxidative cost. Future advance in life‐history theory therefore needs to take account of potential transgenerational impacts of the mechanisms underlying life‐history trade‐offs.     

Impact of modernization on oxidative stress among indigenous populations in northern Laos

Objectives

To explore the impact of modernization on oxidative stress during a momentous health transition process, we investigated differences in oxidative stress among the indigenous populations of villages in northern Laos with different levels of modernization.

Methods

We conducted a cross-sectional study of 380 adults in three villages with different levels of modernization. Three biomarkers related to oxidative stress were measured: urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) and 8-isoprostane concentrations (both measured by liquid chromatography–tandem mass spectrometry), and blood telomere length (measured with qPCR). We examined associations between village-level modernization and oxidative stress-related biomarkers in a multilevel analysis including a random effect and covariates.

Results

The geometric means of urinary 8-OHdG and 8-isoprostane concentrations were 2.92 and 0.700 μg/g creatinine, respectively, in our study population. Higher urinary 8-OHdG concentrations and shorter telomeres were observed in participants from the more modernized villages, whereas urinary 8-isoprostane concentrations did not differ significantly among villages.

Conclusions

Our findings imply that modernization-induced changes in lifestyle may increase oxidative DNA damage. Baseline levels of oxidative lipid damage are expected to be high in the indigenous populations of northern Laos. Assessments of oxidative stress may provide valuable insights into the mechanisms of health transition in specific populations.     

Crickets increase sexual signalling and sperm protection but live shorter in the presence of rivals

The sociosexual environment animals experience through their life can shape the evolution of key life history traits, including longevity. Male–male competition, for instance, may influence the resources allocated to traits involved in male reproductive success. Here, I test whether lifelong exposure to a competitor male influences male investment in pre‐ and post‐copulatory sexual traits (calling effort and sperm quality) and how this affected the oxidative status and longevity of male field crickets (Gryllus bimaculatus). As expected, the visual exposure to a mating competitor promoted a higher calling effort in the male crickets but resulted in a decline in the haemolymph antioxidant content. The haemolymph antioxidant content negatively covaried with the antioxidant content of the sperm but interestingly, only when the males were exposed to a competitor. This suggests that when mating competition is high, males may prioritize sperm antioxidant protection against somatic maintenance. Finally, I provide evidence that male–male competition imposes additional costs to reproduction, as males exposed to a mating competitor lost a significant proportion of body antioxidant defences and body mass over time and in long term, had a reduced lifespan. Overall, this study strongly suggests that intrasexual competition may impose additional oxidative costs during reproduction for males, with negative consequences on lifespan. Moreover, the results highlight the role of oxidative stress as a physiological mechanism underlying the trade‐off between reproduction‐longevity and through which sexual selection may contribute to the evolution of senescence patterns.     

Relationships between hair melanization, glutathione levels, and senescence in wild boars

The synthesis of melanins, which are the most common animal pigments, is influenced by glutathione (GSH), a key intracellular antioxidant. At high GSH levels, pheomelanin (the lightest melanin form) is produced, whereas production of eumelanin (the darkest melanin form) does not require GSH. Oxidative damage typically increases with age, and age-related decreases in GSH have accordingly been found in diverse organisms. Therefore, there should be positive associations between the capacity to produce eumelanic traits, GSH levels, and senescence, whereas there should be negative associations between the capacity to produce pheomelanic traits, GSH levels, and senescence. We explored this hypothesis in a free-ranging population of wild boars Sus scrofa of different ages. As expected from the fact that pheomelanogenesis consumes GSH, levels of this antioxidant in muscle tended to be negatively related to pheomelanization and positively related to eumelanization in pelage, and the degree of pelage pheomelanization was positively related to oxidative damage as reflected by levels of thiobarbituric-acid-reactive substances (TBARS), which is consistent with the hypothesis that pheomelanin synthesis has physiological costs. In our cross-sectional sample, GSH levels did not show senescence effects, and we did not detect senescence effects in pelage melanization. Prime body condition and low TBARS levels were also associated with hair graying, which is attributable to a loss of melanin produced by oxidative stress, thus raising the possibility that hair graying constitutes a signal of resistance to oxidative stress in wild boars. Our results suggest that the degree of melanization is linked to GSH levels in wild boars and that their antioxidant damage shows senescence effects.     

Untangling the oxidative cost of reproduction: An analysis in wild banded mongooses

The cost of reproduction plays a central role in evolutionary theory, but the identity of the underlying mechanisms remains a puzzle. Oxidative stress has been hypothesized to be a proximate mechanism that may explain the cost of reproduction. We examine three pathways by which oxidative stress could shape reproduction. The “oxidative cost” hypothesis proposes that reproductive effort generates oxidative stress, while the “oxidative constraint” and “oxidative shielding” hypotheses suggest that mothers mitigate such costs through reducing reproductive effort or by pre‐emptively decreasing damage levels, respectively. We tested these three mechanisms using data from a long‐term food provisioning experiment on wild female banded mongooses (Mungos mungo). Our results show that maternal supplementation did not influence oxidative stress levels, or the production and survival of offspring. However, we found that two of the oxidative mechanisms co‐occur during reproduction. There was evidence of an oxidative challenge associated with reproduction that mothers attempted to mitigate by reducing damage levels during breeding. This mitigation is likely to be of crucial importance, as long‐term offspring survival was negatively impacted by maternal oxidative stress. This study demonstrates the value of longitudinal studies of wild animals in order to highlight the interconnected oxidative mechanisms that shape the cost of reproduction.     

Reproduction Is Associated with a Tissue-Dependent Reduction of Oxidative Stress in Eusocial Female Damaraland Mole-Rats (Fukomys damarensis)

Oxidative stress has been implicated as both a physiological cost of reproduction and a driving force on an animal''s lifespan. Since increased reproductive effort is generally linked with a reduction in survival, it has been proposed that oxidative stress may influence this relationship. Support for this hypothesis is inconsistent, but this may, in part, be due to the type of tissues that have been analyzed. In Damaraland mole-rats the sole reproducing female in the colony is also the longest lived. Therefore, if oxidative stress does impact the trade-off between reproduction and survival in general, this species may possess some form of enhanced defense. We assessed this relationship by comparing markers of oxidative damage (malondialdehyde, MDA; protein carbonyls, PC) and antioxidants (total antioxidant capacity, TAC; superoxide dismutase, SOD) in various tissues including plasma, erythrocytes, heart, liver, kidney and skeletal muscle between wild-caught reproductive and non-reproductive female Damaraland mole-rats. Reproductive females exhibited significantly lower levels of PC across all tissues, and lower levels of MDA in heart, kidney and liver relative to non-reproductive females. Levels of TAC and SOD did not differ significantly according to reproductive state. The reduction in oxidative damage in breeding females may be attributable to the unusual social structure of this species, as similar relationships have been observed between reproductive and non-reproductive eusocial insects.     

Serum cholesterol positively associated with oxidative DNA damage: a propensity score-matched analysis

Oxidative DNA damage pathogenically links to some major diseases. This study aimed to comprehensively assess the association between serum total cholesterol (TC) and oxidative DNA damage based on propensity score matching (PSM) method. A total of 407 participants chronically exposed to arsenic via drinking water from China were enrolled. Oxidative DNA damage was determined with urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG). Serum TC was classified into favourable TC (FTC, TC <5.18?mmol/L) and unfavourable TC (NFTC, TC ≥5.18?mmol/L) categories. Multivariable generalised linear regression model was applied to examine the association. Of 407 participants, 125 pairs with FTC and NFTC subjects were matched using PSM. Urinary 8-OHdG/creatinine levels in NFTC were significantly higher than those in FTC category (p?=?.002). As compared to the counterparts, additional adjusted log-transformed 8-OHdG/creatinine increase was observed in NFTC for unmatched (β?=?0.12, p?=?.052) and matched (β?=?0.17, p?<?.001) participants, respectively. We also detected obviously increased log-transformed urinary 8-OHdG/creatinine with per interquartile range raise of serum TC either in unmatched (β?=?0.10, p?=?.007) or matched (β?=?0.16, p?=?.003) subjects. In conclusion, serum TC was independently associated with oxidative DNA damage. Our findings provided new insights on the health promotion of lipids relevant to the early warning of diseases due to oxidative DNA damage.     

Is oxidative stress a physiological cost of reproduction? An experimental test in house mice

Investment in reproduction is costly and frequently decreases survival or future reproductive success. However, the proximate underlying causes for this are largely unknown. Oxidative stress has been suggested as a cost of reproduction and several studies have demonstrated changes in antioxidants with reproductive investment. Here, we test whether oxidative stress is a consequence of reproduction in female house mice (Mus musculus domesticus), which have extremely high energetic demands during reproduction, particularly through lactation. Assessing oxidative damage after a long period of reproductive investment, there was no evidence of increased oxidative stress, even when females were required to defend their breeding territory. Instead, in the liver, markers of oxidative damage (malonaldehyde, protein thiols and the proportion of glutathione in the oxidized form) indicated lower oxidative stress in reproducing females when compared with non-reproductive controls. Even during peak lactation, none of the markers of oxidative damage indicated higher oxidative stress than among non-reproductive females, although a positive correlation between protein oxidation and litter mass suggested that oxidative stress may increase with fecundity. Our results indicate that changes in redox status occur during reproduction in house mice, but suggest that females use mechanisms to cope with the consequences of increased energetic demands and limit oxidative stress.     

Oxidative stress markers in patients with post-traumatic stress disorder

Recent study data support the role of oxidative stress in diverse psychiatric disorders. Oxidative stress results from an oxidant/antioxidant imbalance, an excess of oxidants and/or a depletion of antioxidants. There are numerous studies that indicate that free radicals (FRs) damage neurons, and then play an important role in the pathophysiology of schizophrenia and depression. Active oxygen can cause considerable damage and disrupt the important physiological functions of proteins, lipids, enzymes and DNA. The aim of our study was to investigate the possible differences in the concentration of tromboxane B2, 8-OHdG and protein carbonyls, as significant markers of oxidative damage, and urate, albumin and total protein concentrations as antioxidative molecules in PTSD patients in comparison to the healthy control group. The study included 74 male participants who were active soldiers in the Croatian armed forces from 1991 to 1995. 46 subjects with chronic and current PTSD were recruited from the Department of Psychiatry of Dubrava University Hospital during 2010, 28 healthy subjects were recruited in the same period during the regular medical examination at the Dubrava University Hospital. Study results have shown that there is no statistically significant difference in urinary concentrations of 8-OHdG, serum thromboxane B2, and serum urates between two studied groups. Statistically significant difference of the protein carbonyl concentrations was examined. Concentrations were significantly lower in the PTSD group than in the control group. The clinical significance of these results was examined using ROC analysis. The obtained ROC curves did not separate the groups in a satisfactory manner.     

Association of serum arginase I with oxidative stress in a healthy population

The association of serum arginase I with oxidative stress was evaluated cross-sectionally in a healthy population. The mean levels of serum arginase I in healthy people (n = 278) were 32.6 ± 22.3 ng/ml. Significant correlations of arginase I were observed with age, WBC, RBC, alanine aminotransferase (ALT), high-sensitivity C-reactive protein (hs-CRP), uric acid, body mass index (BMI) and urinary 8-isoprostane. Multiple regression analysis showed significant associations of arginase I with WBC, RBC, urinary 8-hydroxydeoxyguanosine (8-OHdG), age, HbA1c and urinary 8-isoprostane. In the associations of arginase I with 8-OHdG, 8-isoprostane and HbA1c, confounding factors and lifestyle factors such as sex, old age, smoking and alcohol consumption were involved. It was concluded that serum arginase I was associated with oxidative stress and HbA1c in addition to age, WBC and RBC in healthy Japanese people and may become a new biomarker for early prediction of diabetes mellitus and other oxidative stress-related diseases.     

Detection of oxidative DNA damage in human sperm and its association with sperm function and male infertility

The expanding research interest in the last two decades on reactive oxygen species (ROS), oxidative stress, and male infertility has led to the development of various techniques for evaluating oxidative DNA damage in human spermatozoa. Measurement of 8-hydroxydeoxyguanosine (8-OHdG) offers a specific and quantitative biomarker on the extent of oxidative DNA damage caused by ROS in human sperm. The close correlations of 8-OHdG level with male fertility, sperm function and routine seminal parameters indicate the potential diagnostic value of this technique in clinical applications. On the other hand, single cell gel electrophoresis (SCGE or comet assay) and terminal deoxynucleotidyl transferase (TdT) mediated dUTP nick end labeling (TUNEL) assay have also been demonstrated to be sensitive, and reliable methods for measuring DNA strand breaks in human spermatozoa. As certain technical limitations were inherent in each of these tests, it is believed that a combination of these assays will offer more comprehensive information for a better understanding of oxidative DNA damage and its biological significance in sperm function and male infertility.     

The developing reproductive 'sink' induces oxidative stress to mediate nitrogen mobilization during monocarpic senescence in wheat

Removal of reproductive 'sink,' i.e., spikelets from wheat, after anthesis delays the rate of flag leaf senescence. Oxidative stress and the oxidative damage to proteins were studied in relation to nitrogen mobilization in wheat plants showing normal and delayed senescence. Wheat plants lacking a reproductive sink showed decreased oxidative stress, lower lipid peroxidation and maintained higher protein, oxidatively damaged proteins, and nitrogen levels as compared to plants with reproductive sink during monocarpic senescence. Oxidative damage to the proteins when not followed by high proteolytic activities led to a slower nitrogen mobilization in wheat plants lacking a reproductive sink. Thus, the influence of the reproductive sink was due to its ability to drive forward the nitrogen mobilization process through high ROS levels which mediated both damage to the proteins and influenced proteolytic activities.     

Inorganic arsenic compounds cause oxidative damage to DNA and protein by inducing ROS and RNS generation in human keratinocytes

Arsenic is a naturally occurring element that is present in food, soil, and water. Inorganic arsenic can accumulate in human skin and is associated with increased risk of skin cancer. Oxidative stress due to arsenic exposure is proposed as one potential mode of carcinogenic action. The purpose of this study is to investigate the specific reactive oxygen and nitrogen species that are responsible for the arsenic-induced oxidative damage to DNA and protein. Our results demonstrated that exposure of human keratinocytes to trivalent arsenite caused the generation of 8-hydroxyl-2′-deoxyguanine (8-OHdG) and 3-nitrotyrosine (3-NT) in a concentration- and time-dependent manner. Pentavalent arsenate had similar effects, but to a significantly less extent. The observed oxidative damage can be suppressed by pre-treating cells with specific antioxidants. Furthermore, we found that pre-treating cells with Nω-nitro-l-arginine methyl ester (l-NAME), an inhibitor of nitric oxide synthase (NOS), or with 5,10,15,20-tetrakis (N-methyl-4′-pyridyl) porphinato iron (III) chloride (FeTMPyP), a decomposition catalyst of peroxynitrite, suppressed the generation of both 8-OHdG and 3-NT, which indicated that peroxynitrite, a product of the reaction of nitric oxide and superoxide, played an important role in arsenic-induced oxidative damage to both DNA and protein. These findings highlight the involvement of peroxynitrite in the molecular mechanism underlying arsenic-induced human skin carcinogenesis.     

Oxidative damage increases and antioxidant gene expression decreases with aging in the mouse ovary

Oxidative stress has been implicated in various aspects of aging, but the role of oxidative stress in ovarian aging remains unclear. Our previous studies have shown that the initiation of apoptotic cell death in ovarian follicles and granulosa cells by various stimuli is initiated by increased reactive oxygen species. Herein, we tested the hypothesis that ovarian antioxidant defenses decrease and oxidative damage increases with age in mice. Healthy, wild-type C57BL/6 female mice aged 2, 6, 9, or 12 mo from the National Institute on Aging Aged Rodent Colony were killed on the morning of metestrus. Quantitative real-time RT-PCR was used to measure ovarian mRNA levels of antioxidant genes. Immunostaining using antibodies directed against 4-hydroxynonenal (4-HNE), nitrotyrosine (NTY), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) was used to localize oxidative lipid, protein, and DNA damage, respectively, within the ovaries. TUNEL was used to localize apoptosis. Ovarian expression of glutathione peroxidase 1 (Gpx1) increased and expression of glutaredoxin 1 (Glrx1), glutathione S-transferase mu 2 (Gstm2), peroxiredoxin 3 (Prdx3), and thioredoxin 2 (Txn2) decreased in a statistically significant manner with age. Statistically significant increases in 4-HNE, NTY, and 8-OHdG immunostaining in ovarian interstitial cells and follicles were observed with increasing age. Our data suggest that the decrease in mRNA expression of mitochondrial antioxidants Prdx3 and Txn2 as well as cytosolic antioxidants Glrx1 and Gstm2 may be involved in age-related ovarian oxidative damage to lipid, protein, DNA, and other cellular components vital for maintaining ovarian function and fertility.     

CSR ecological strategies and plant mating systems: outcrossing increases with competitiveness but stress‐tolerance is related to mixed mating

A number of plant traits influence the success of fertilization and reproduction in plants. Collectively these traits represent ecological syndromes that are of evolutionary significance. However, while an association between mating system and colonizing ability has been proposed, the existence of a broader relationship between mating system and a species’ position in ecological succession has not been extensively investigated. Grime's CSR theory stresses that an ecological succession can involve changes from colonizing to either competitive or stress‐tolerant strategies. How distinct dimensions of competitiveness and stress tolerance covary with mating systems has still not been considered. We designed a comparative approach to evaluate the link between mating system, life form and CSR strategies for 1996 herbaceous and woody species. We found that CSR strategies are significantly related to mating systems. Ruderal species – colonizers in early succession – were mostly selfers while more competitive species were more often outcrossers. On the other hand, greater physiological stress tolerance was associated with mixed mating systems. Outcrossing is classically expected to be advantageous for most life history strategies other than colonizers, but we suggest that reproductive assurance can counterbalance this effect in stressful environments where populations are sparse and pollinators are rare. Therefore, our results emphasize that competition and abiotic stresses are not equivalent selective pressures on the evolution of mating systems. Finally, we found plant life span to convey additional information on mating system variation, supporting its role for mating system evolution. These findings encourage further investigation of the evolutionary role of ecological strategies as syndromes of traits and suggest that the emergence of large databases of plant traits will help address the major evolutionary hypotheses on such syndromes.