**2. Physiological mechanism of plants under water deficit**

With the advancement of global climate change, the occurrence of longer periods of water deficiency becomes more frequent, causing climatic risks to plant growth and, consequently, to agricultural activity. In the environmental context, prolonged periods without precipitation cause a reduction in soil water content and a decrease in vegetation growth, except in plants adapted to conditions of water scarcity, a fact quite common in arid and semi-arid regions. In the semi-arid region of northeastern Brazil, the occurrence of prolonged periods of water scarcity is common, with a drastic reduction in the availability of water in the soil, with the permanence of only species adapted to the semi-arid climate (**Figure 1**).

Physiologically, plants under water stress manifest a set of responses that culminate in reduced plant growth. Thus, the decrease in water availability induces stomatal closure due to greater synthesis and physiological action of abscisic acid on stomata. These close as a physiological strategy to reduce water loss through perspiration. This physiological phenomenon induces stomatal limitation to photosynthesis due to the reduction in the intercellular concentration of carbon dioxide [11].

The drop in the intercellular concentration of carbon dioxide can decrease the consumption of ATP and the NADPH2 reducing power by the Calvin cycle, allowing electrons from the electron transport chain to interact with free molecular oxygen forming superoxide radicals, since NADPH2 is chemically reduced (**Figure 2**).

*Toxic Aluminum and Water Deficit Interaction in Plants: Physiological Aspects and Chemical… DOI: http://dx.doi.org/10.5772/intechopen.111418*

#### **Figure 1.**

*Effect of rainfall seasonality on vegetation. (A) Atriplex nummularia in dry soil; (B) soils with cracks due to periods of intense water deficit; (C) plants tolerant to water deficit in the rainy season and (C) in the dry season. Images recorded in the semi-arid region. Northeast Brazil. Source: Author.*

#### **Figure 2.**

*Stomatal closure in response to water deficiency: Water deficiency induces the synthesis of abscisic acid in the root and leaves. ABA modulates stomatal closure, which reduces gas exchange. The decrease in CO2 diffusion implies less consumption of NADPH2 by the Calvin cycle. This allows O2 to react with electrons from the electron transport chain and there is the formation of free radical O2 − in the vicinity of photosystem I, triggering oxidative stress. Source: Author.*

This set of events culminates in oxidative stress that causes lipid peroxidation and important cellular damage in plants under water deficit [12]. However, although water deficiency reduces the carboxylation activity of the enzyme RUBISCO (ribulose 1,5-bisphosphate carboxylase-oxygenase), its oxygenase function is increased, which allows temporary consumption of NADPH2 and ATP, reducing the production of reactive oxygen species (ROSs). However, photorespiration allows the recycling of phosphoglycolate (a toxic compound) to phosphoglycerate during carbon fixation [13, 14].

Despite the cellular damage caused by ROS, they have a dual role in cells because they participate in cell signaling, but they are also toxic products of aerobic metabolism in plants [15, 16]. The main free radicals produced in plants under water deficit are the superoxide radical (O2 − ), peroxide radical (H2O2), and hydroxyl radical (OH− ). The O2 − radical is synthesized in the apoplast, chloroplast, mitochondria, peroxisomes, and electron transport chain. The H2O2 radical, in turn, can be synthesized in peroxisomes, chloroplasts, mitochondria, cytosol, apoplast, and cytosol. The OH<sup>−</sup> radical is synthesized from the H2O2 radical according to Fenton's reaction [16]. The oxidative stress resulting from water deficiency, in addition to increasing lipid peroxidation, reduces photosynthetic activity due to the harmful action of ROS on the photosynthetic machinery causing photoinhibition [17].

The mineral metabolism of plants is considerably affected by water deficiency, especially by nutrients that are absorbed through mass flow such as nitrogen [18]. The key enzyme present in plants that allows the entry of nitrogen into plants is nitrate reductase (RN, EC 1.6.6.1) which converts nitrate (NO3 − ) to nitrite (NO2 − ). One of the environmental factors that modulate the activity of the RN enzyme is the availability of nitrate, which is absorbed by the root system via transpiration [19]. Thus, water deficiency is a factor that indirectly decreases NR activity, because it limits the absorption of nitrate by the roots [20].

Water deficiency imposes limitations on plants regarding the acquisition of water in the environment in which they live since with the advancement of water restriction, the water potential of the soil tends to become more negative. In this sense, plants must maximize water use to avoid excessive loss through transpiration and maintain their water status favorable to their physiological activities. A biochemical strategy aimed at tolerating water deficiency is the synthesis of compatible osmolytes, which reduce the cellular osmotic potential for water influx into cells. Furthermore, compatible osmolytes preserve the conformational structure and maintain the biological activity of biomolecules [21, 22]. Amino acids (proline, glycine betaine, gamma-aminobutyric acid) and carbohydrates (sorbitol, sucrose, trehalose, mannitol, and raffinose) are compatible osmolytes used by plants during water deficit for osmotic adjustment and improvement of water status [21, 23]. Proline and glycine betaine are two important compatible osmolytes involved in modulating the response of plants to water stress [24, 25].

It should be emphasized that there is a negative correlation between the water content and the concentration of compatible osmolytes in plants under water deficit. However, increases in the concentration of compatible osmolytes do not necessarily imply an increase or stability in the plant growth rate in the face of water restriction experienced by the plants [7].

### **3. Physiological mechanisms of aluminum toxicity in plants**

Metal toxicity is one of the world's biggest problems for agricultural production. Some metals are not essential to plants but are very toxic when present in certain forms in soil. Among metals, aluminum (Al) is one of the most toxic because it reduces the growth and production of many crops in acidic soils [26]. Around 50%

*Toxic Aluminum and Water Deficit Interaction in Plants: Physiological Aspects and Chemical… DOI: http://dx.doi.org/10.5772/intechopen.111418*

of arable land in the world is acidic [27] and around 60% of acidic soils are found in tropical and subtropical regions because in these regions the soil acidification process is natural [28].

The absorption of Al via symplast or apoplast can cause injuries to biomolecules in the cell wall, membrane, cytoplasm, and nucleus, affecting the structure of root cells and, consequently, the ability of root cells to absorb water and mineral salts from the soil [28]. Al bound to root cells appears to be localized to the apoplast cell wall and plasma membrane surface [29]. Therefore, the toxic effect of Al results from its external connection with root cells [27]. Thus, the initial site of Al toxicity occurs in the roots, which present physiological and biochemical changes that result in reduced root growth (**Figure 3**).

The physiological activity of the root system is affected by Al as it is the initial site of toxicity for this toxic metal. Thus, the ability to absorb water and mineral nutrients is compromised by toxic levels of Al. Therefore, toxic Al affects water relations in plants, reducing transpiration, water use efficiency, and intrinsic water use efficiency [30]. In addition, transpiration, root hydraulic conductivity, and leaf water potential are negatively affected by Al and these disorders in plant water relations coincide with increased levels of ABA in plants treated with toxic Al, indicating that this metal has a broad spectrum of action. Physiology in plants [31].

The mineral metabolism of plants is affected by the toxic action of Al, because this toxic metal inhibits the activity of the nitrate reductase enzyme and, consequently, the conversion of nitrate to nitrite in plants. In addition, Al reduces the levels of macronutrients (calcium, magnesium, phosphorus, and potassium) inducing nutritional disorders in plants that result in reduced plant growth [32, 33].

Although there is a greater accumulation of Al in the root system than in the aerial part of the plants, the physiological activity of the leaves is considerably affected by Al. This metal reduces the concentration of chlorophylls and, consequently, the

**Figure 3.**

*Toxic aluminum primarily targets the root system. Aluminum concentrations above 4 mmol L−1 severely reduce root and shoot growth of Cajanus cajan seedlings. Source: Author.*

**Figure 4.**

*Aluminum-modulated free radical production and programmed cell death in mitochondria. Aluminum activates the NADPH oxidase located in the mitochondrial membranes, inducing the overproduction of free radicals (O2 − and H2O2) accelerating programmed cell death. Source: Figure adapted from hung et al. [39].*

photosynthetic activity [34]. Al reduces the rate of photosynthesis because it is harmful to the functioning of the photosynthetic machinery by inhibiting electron transport mediated by photosystems I and II [34–36] and the carboxylate activity of the enzyme RUBISCO [37]. This negative effect of Al is reinforced by the fact that free radical production is located close to the reaction center of photosystems I and II of thylakoids in chloroplasts [15].

Al toxicity induces the production of O2 − , H2O2, and OH- both in shoots and roots, causing lipid peroxidation and electrolyte leakage in plants [34, 38–40]. Although Al triggers oxidative stress in plants [34], the mechanism itself is indirect because Al activates NADPH oxidase (**Figure 4**) one of the main sources of ROS generation in plants under Al stress [39].

Respiratory burst oxidase homolog proteins (RBOHS) are integral plasma membrane proteins. They are formed by six transmembrane domains that support two heme groups, C-terminal FAD and NADPH hydrophilic domains, and two N-terminal calcium-binding domains (EF-hand). NADPH oxidase acts as a cytosolic electron donor to the extracellular O2 electron acceptor, which is reduced to O2 − via FAD and two independent hemes [41].
